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PSYCHOLOGICAL ADJUSTMENT AND SYSTEMIC LUPUS ERYTHEMATOSUS:
AC 0 M PARATIVE STUDY
Helen Hornsby B.A. (Hons.)
Report submitted as a partial requirement for the degree of Master of Psychology (Clinical)
DEPARTMENT OF PSYCHOLOGY UNIVERSITY OF TASMANIA
Sep'terii.ber, 1993
Itiki.AcSII 4 yilASISc)
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SOURCES STATEMENT
The present thesis describes original research undertaken in the
Department of Psychology, University of Tasmania. To the best of my
knowledge, any theories and techniques not my own have been
acknowledged in the text. The remaining theoretical contributions in
this thesis are my own original work and have not been submitted for
any other degree.
Signed:
Helen Hornsby
ABSTRACT
Systemic lupus erythematosus (SLE) is a chronic inflammatory
disease of unknown etiology. Its affects multiple organ systems and
is characterised by periods of disease activity and remission. The
unpredictable course, treatment and symptomatology of SLE can
impact upon the social and personal resources of sufferers. Social
resources are those variables influenced by external events, they
include stress, uplifts, social support and social networks. Personal
resources are mediated more by individuals' perceptions and
include self—efficacy and coping (problem— and emotion—focused).
Deteriorations in social and personal resources accompanying
chronic illness suggest a Disease Exacerbation Model. This model
proposes that the course of chronic illness is mediated by
decrements in social and personal resources which, in turn,
influence disease outcomes such as physical disability, psychosocial
disruption and psychological distress.
The present investigation used a comparative design to test the
Disease Exacerbation Model. The participants in the study were 34
individuals with a diagnosis of SLE, 37 multiple sclerosis (MS)
sufferers and 38 people without a history of chronic illness. The
control group was matched to the chronic illness groups for age,
marital status, gender and socioeconomic status. Data were
collected by using standardised psychological questionnaires. These
included measures of stress, hassles, social network, social support,
self-efficacy, coping, psychological distress, physical disability and
psychosocial disruption.
Individuals with SLE and a chronic illness comparison group (MS)
reported significantly fewer uplifts, less social support, more
emotion—focused coping, as well as greater disability, distress and
psychological disruption when compared with healthy people.
There were, however, no significant decrements in network size or
problem—focused coping and no significant increases in hassles.
Except for the MS group reporting significantly more disability than
SLE sufferers, no other differences were evident between the
chronic illness groups. The correlations between social, personal
and disease outcome measures suggest that group differences may
involve somewhat different underlying processes. For example,
social support mediated psychological distress for SLE sufferers, but
not for the MS group.
To determine which social and personal resource variables are most
salient to disease outcome, stepwise multiple regression analyses
were performed. For SLE sufferers, increasing hassles and fewer
uplifts were associated with elevated psychological distress.
Although higher hassle levels and decreasing social support were
both correlated with more psychosocial disruption, in the stepwise
regression only hassles significantly predicted this disease outcome.
Physical disability levels were not significantly related to any social
or personal resource measures.
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ACKNOWLEDGEMENTS
Of the many involved in the unrewarding task of supervising a
languorous student such as myself, I wish to acknowledge John
Davidson, Christine Clifford, lain Montgomery and Christopher
Williams. The word—grubber (alias Barry Mapperson) also deserves
thanks, as his guidance lead to the metamorphosis of my writing style.
I am also indebted to Christine Clifford, Maurice Gourlay and Shirin
Fernandez for assisting in proofing and editing. Finally, I wish to
thank those volunteers who forfeited their coffee and time to
complete the questionnaires.
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TABLE OF CONTENTS
Sources Statement
Abstract ii
Acknowledgements iv
Table of Contents
List of Tables vii
List of Figures viii
CHAPTER ONE: Systemic Lupus Erythematosus: An Overview 1 1.1.0 Introduction 2
Description 2
Pathogenesis 2
Symptomatology 4
Disease Course 6
Diagnosis 7
Epidemiology 10
Etiology 11
Treatment 13
Medical Aspects and Psychological Adjustment 17
1.1.1 Summary 17
CHAPTER TWO: Psychological Adjustment and Systemic Lupus Erythematosus 19
2.0.0 Overview 20
2.1.0 Social Resources 20
2.1.1 Stress 21
Stress and Immune Functioning 21
Measurement 25
Life Events and Daily Hassles 26
Life Events, Hassles and SLE Research 28
Summary 30
2.1.2 Social Networks and Social Support 31
Models 32
The Link Between Social Relationships and Disease Outcomes 33
Measurement Issues 35
Social Relationships and Autoimmune Disease Research 36 Summary 38
2.2.0 Personal Resources 39
2.2.1 Self—Efficacy 39
Theory Refinements 41
Relationship to Other Personal Resources 43
Self—Efficacy and Autoimmune Disease Research 45
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2.2.2 Coping 48 Theory 48 Coping and Autoimmune Disease Research 50
2.3.0 Disease Outcome Measures 54 2.3.1 Psychological Distress 54
Incidence and Syndromes 55 Etiology 57
2.3.2 Functional Disruption Measures 59
2.4.0 Chapter Summary 61 2.5.0 Hypotheses 66
CHAPTER THREE: Method 68 3.1.0 Design 69 3.2.0 Participants 69 3.3.0 Questionnaires 71
Social Resources 72
Personal Resources 74
Disease Outcome 75
3.4.0 Procedure 79
CHAPTER FOUR: Results 82 4.1.0 Group Comparisons 82
4.2.0 Relationships Between Variables 86 4.3.0 Predicting Disease Outcomes 87
CHAPTER FIVE: Discussion 92
5.1.0 Overview 93
5.2.0 Group Comparisons 93
Social Resources 93
Personal Resources 99
Disease Outcome Measures 102
5.3.0 Predictors of Disease Outcome 104
Psychological Distress 104 Physical Disability 105 Psychosocial Disruption 105
5.4.0 Summary and Conclusion 106
References
109 Appendix One: Questionnaires
119
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LIST OF TABLES
Cellular components of the immune system. 3
Demographic characteristics of subjects. 71
Problem—focused and emotion—focused COPE subscales. 77
Table 4: The SCL-90—R symptom dimensions and global distress indices. 78
Examples of items comprising the physical and psychosocial disruption subscales. 80
Mean and standard deviation scores for social, personal and disease outcome measures. 85
Table 1:
Table 2:
Table 3:
Table 5:
Table 6:
Table 7:
Table 8:
Table 9:
Univariate comparisons and post hoc tests for social, personal and disease outcome measures for the control (C), SLE and MS groups.
Correlation Matrices for SLE, MS and control groups.
Summary of stepwise regression for variables predicting psychosocial distress.
86
88
89
Table 10: Summary of stepwise regression for variables predicting physical disability levels. 90
Table 11: Summary of stepwise regression for variables predicting psychosocial disruption. 91
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LIST OF FIGURES
Figure 1: Medical approaches for assessing health outcomes. 60
1
Chapter One
Systemic Lupus Erythematosus: An Overview
2
1.1.0 INTRODUCTION •
This section reviews the medical aspects of systemic lupus
erythematosus (SLE or lupus). It is included to familiarise the reader
with the symptomatology, treatment and etiology of lupus. The
chapter also provides the foundations for understanding research
reviewed in later sections and discusses how the physical
characteristics of SLE may precipitate psychological dysfunction.
DESCRIPTION
A concise and informative description of SLE is provided by Wallace
and Dubois (1987);
"Systemic lupus erythematosus is a clinical syndrome
of unknown cause or causes characterised by
inflammation and multisystem involvement. It
displays a widely variable presentation and course
and is subject to multiple remissions and
exacerbations in one or more systems. In
approximately 30% of cases, the disease is induced by
known drugs."
(p.15)
PATHOGENESIS
To understand the pathogenesis of SLE it is necessary to briefly explain
how the immune system functions. Whenever foreign organisms
[antigens] such as viruses or bacteria invade, the immune system is
mobilised. The first line of defence involves phagocytes engulfing
3
and digesting antigens (O'Donnnell, Silove & Wakefield, 1988; Table
1). When the antigen is digested, phagocytes bind with antigen
presenting cells. These latter cells then incorporate the nuclear
material of the antigen into their membrane so it may be recognised
by other immune defences.
Table 1: Cellular components of the immune system. (after O'Donnnell et al., 1988)
1. Phagocytes monocytes macrophages polymorphonucle neutrophils
2. Antigen Presenting cells monocytes macrophages accessory cells
3. T—lymphocytes regulatory cells helper cells suppressor cells effector cells delayed hypersensitivity cytotoxic T—lymphocytes
4. Natural Killer cells
5. B—lymphocytes plasma cells memory cells
When antigen presenting cells bind with T—lymphocyte helper cells
interleukin-1 is secreted (Hardy, 1985). Interleukin-1 causes the
proliferation of helper cells and these secrete interleukin-2 which has
several functions. It stimulates T—suppressor cells that switch off the
4
immune response when the time is appropriate. Interleukin-2 also
stimulates the reproduction of T-killer cells that will either bind with
the antigen presenting cell or engulf the antigen directly. Finally,
interleukin-2 stimulates B-lymphocytes to produce antibodies
(immunoglobulins) that bind with the invading antigen so it is easily
recognised by T-cells. B-lymphocytes are antigen specific and if the
antigen invades again, they are mobilised immediately (Blau &
Schultz, 1984).
Autoimmune diseases are characterised by immune attacks toward
native body proteins. In lupus the immune attacks are directed
toward deoxyribonucleic acid (DNA or the genetic material of cells).
Since all cells contain DNA, every organ is a potential target for
immune attacks. Although the etiology of immune attacks is not
known, immune irregularities associated with SLE are well
documented. Individuals with SLE have lower interleukin-2 levels,
suppressor cells fail to switch-off the immune system and
B-lymphocytes are constantly active whether or not there is infection
(Blau & Schultz, 1984).
SYMPTOMATOLOGY
Since all organs are at risk in SLE, there is no typical presentation of
patients. Signs and symptoms of SLE are, however, characterised by
inflammation and include arthritis, rashes, kidney involvement and
fevers (Schur, 1983; Hardy, 1985).
5
The most common symptom of SLE is inflammation of the synovial
membrane that surrounds the joints (Schur, 1983). This occurs in
about 90 percent of sufferers and differs from rheumatoid arthritis in
that joint deformity is rare. Often accompanying joint involvement is
inflammation of the tendons and muscles which occurs in about 15
percent of lupus sufferers.
The skin is affected in over 70 percent of individuals with SLE (Hardy,
1985). Rashes may be present on the hands, feet or face and arise from
inflammation of arterioles. A butterfly rash over the cheeks and nose
bridge occurs in about 40 percent of patients. About 15 percent of
individuals have discoid lesions. These are red, blotchy, scaly sores
that may leave scaring upon healing.
Inflammation of the kidneys can result in protein and blood in the
urine and is a significant cause of death in SLE sufferers (Schur, 1983).
If the membrane that surrounds the lungs becomes inflamed, sharp
stabbing pains on taking a deep breath may result. Pericarditis occurs
when the pericardium membrane encasing the heart becomes
inflamed. The symptoms of pericarditis mimic myocardial infarction
and include shortness of breath, ankle swelling and breathing
difficulties after exercise or when lying down.
Raynaud's phenomenon is similar to frostbite but occurs in the
absence of cold weather (Blau & Schultz, 1984). It results from
inflammation of arterioles that supply blood to the fingers and occurs
6
in about 15 percent of sufferers. Sjogren's syndrome occurs in 40
percent of patients and results from reduced gland secretions.
Other signs and symptoms of SLE include anaemia, seizures,
psychoses, damage to the retina, temporary hair loss and mouth
ulceration. Fevers, light sensitivity (photosensitivity), generalised
aching and fatigue also are common. Gastrointestinal problems such
as constipation, diarrhoea, nausea and vomiting are evident in 40
percent of sufferers (Blau & Schultz, 1984; Hardy, 1985).
Despite the diversity of SLE symptoms, rarely do individuals
experience more than five or six of those described above.
Furthermore, while organs such as the heart and kidneys may become
involved, the majority of sufferers do not experience such
complications. Regardless of the symptoms that arise, SLE can be
debilitating as symptoms disrupt life-style causing sufferers
considerable psychological distress.
DISEASE COURSE
The symptomatology of SLE is characterised by periods of flare and
remission (Blau & Schultz, 1984; Hardy, 1985). A disease flare
occurs when symptoms increase in intensity and there is
inflammation of the affected organs. Remission occurs when
symptoms become more quiescent and inflammation is reduced.
Since SLE is a chronic disorder, remission does not necessitate the
absence of inflammation or symptomatology, rather symptom
intensity is merely reduced (Hardy, 1985).
7
Since prognosis depends on numerous factors such as the severity
of the disease, the organs effected, age and response to therapy, it is
difficult to predict the course of SLE. Improved diagnostic
strategies and pharmacological management are, however,
contributing to an increasing survival rate, with the result that life
expectancy has doubled in the last 20 years (Schur, 1983). In 1953,
for example, the five year survival rate was less than 40 percent. In
a 1987 study over 80 percent of individuals were alive nine years
after diagnosis (Studenski, Allen, Caldwell, Rice & Polisson, 1987).
Despite an increasing life expectancy and treatment advances, the
major causes of mortality remain unchanged. These are
progressive renal failure, central nervous system (CNS) symptoms
and superimposed infections (Kinash, 1983; Studenski, et al., 1987;
Wallace & Dubois, 1987).
Although SLE is sometimes life—threatening, the majority of
individuals survive well into the sixth decade ( Wallace & Dubois,
1987). Nonetheless, the prospect of kidney or CNS involvement or
a poor prognosis remains a concern for many sufferers.
Occasionally such concerns may disrupt social and occupational
functioning and cause considerable psychological distress (Hardy,
1985).
DIAGNOSIS
Systemic lupus erythematosus mimics the symptomatology of other
diseases (Kinash, 1983). For example, it is common for individuals to
present with evidence of arthritis, but there is no joint deformity
8
when x—rayed. Similarly, chest pains suggesting heart disease may be
reported, but there are no electrocardiogram abnormalities. •The
pathogenesis and flaring and remitting course of SLE can make
diagnosis difficult. Only when symptoms appear then disappear is the
condition suspected and because symptoms can take years to appear,
diagnosing the condition also may take years.
A RA CRITERIA
In 1971 the American Rheumatism Association (ARA) published
preliminary diagnostic criteria to clarify the parameters of SLE
( Wallace & Dubois, 1987). These criteria were revised in 1982 to
achieve a diagnostic sensitivity and specificity rate of 96 percent
(Schur, 1983). An individual has SLE if they meet four of the 11
criteria (Appendix one) and is given a probable diagnosis if they meet
three. Symptoms need not be present simultaneously and a patient's
medical history is considered when reaching a diagnosis. It takes an
average of three years for a patient to meet four ARA criteria ( Wallace
& Dubois, 1987).
Despite the high reported sensitivity and specificity of the ARA
criteria, the taxonomy has several limitations. It excludes important
signs of SLE such as alopecia (hair loss), Raynaud's phenomena,
persistent low grade fevers and fatigue. The criteria were derived
from a small sample of SLE sufferers and from retrospective studies
( Wallace & Dubois, 1987). The ARA scheme also may eliminate some
individuals from an 'official' diagnosis, as it does not weight the
importance of symptoms. For example, individuals could have
9
definitive symptoms such as immunological disorder, antinuclear
antibodies and a discoid rash but would not be diagnosed with SLE as
they met only three criteria.
Since the present study is not concerned with the medical diagnosis of
SLE, the ARA scheme will be modified for recruiting volunteers. In
this study, an individual has SLE if they meet (a) three ARA criteria
and their treating physician has diagnosed SLE, or (b) have
immunological disorder, antinuclear antibodies and one other ARA
diagnostic symptom.
DIFFERENTIAL DIAGNOSIS
Discoid skin lesions in the absence of subcutaneous symptoms is
diagnosed as discoid lupus erythematosus (DLE) rather than SLE.
Discoid lupus is characterised by localised inflammation of the skin,
often occurring in areas exposed to solar or ultraviolet irradiation.
This condition is persistent but not life-endangering, although in
some cases SLE develops (Hardy, 1985).
A lupus-like syndrome also may be induced by several classes of drug,
including cardiovascular, antimicrobial, anticonvulsant and
psychotropic medications (Schur, 1983). Drug-induced SLE differs
from the idiopathic variety in several ways. It does not favour
women more than men. Nephritis (inflammation of the kidneys)
and central nervous system features are not ordinarily present.
Antibodies to several classes of proteins are less common in
drug-induced lupus. Finally, false-positive tests to syphilis (ARA
10
criteria 10) disappear when the offending drug is withdrawn (Krupp &
Schroeder, 1987). In about 30 percent of individuals, however, the
offending medications precipitate the idiopathic condition, suggesting
some individuals have a pre—existing diathesis for SLE (Harmon &
Portanova, 1982).
EPIDEMIOLOGY
Several studies confirm the incidence of SLE is between 2.6-4.6 per
100,000 with a prevalence rate of 1 per 6780 (Meddings & Grennan,
1980; Wallace & Dubois, 1987). The ratio of women to men sufferers is
reported as 9:1, although this varies with age. Below the age of 15 and
above 60 this ratio is somewhat lower, with about twice as many
females suffering from SLE as males. Explanations for the gender
difference rates include loss of male siblings at birth, environmental
and hormonal factors. These will be discussed further in the etiology
section. Reported onset ages range from three months to 87 years,
however most cases have their onset between 15 and 45 years. The
average onset age is 28 years for females and 51 years for males.
Higher rates of SLE have been reported in black Americans, Hispanics,
Chinese and Indian populations ( Wallace & Dubois, 1987). Racial and
geographic differences are however a likely consequence of sampling
strategies and diagnostic practices. Studies comparing black with
white Americans, for example, report threefold prevalence rates in
the former group. Yet the prevalence rate for black Africans is
comparable to that of white Americans. Another explanation for
racial patterns stems from naturally differing levels of blood
11
constituents. Blacks, for example, have naturally higher levels of
gamma globulins than whites (Wallace & Dubois, 1987). Differing SLE
spectrum definitions also explain contrary prevalence rates.
American studies that use ARA diagnostic criteria may exclude SLE
sufferers, whereas Asian and Indian definitions are more inclusive
( Wallace & Dubois, 1987).
ETIOLOGY
While the pathogenesis is well documented, less is known about the
causes of lupus. It is likely, however, that lupus arises from a
combination of hormonal, genetic and viral causes. These are briefly
considered below and the interested reader is referred to Wallace and
Dubois (1987) for an extensive review.
HORMONAL
Autoimmune conditions occur more often in women because they
are more immunologically reactive than men (Talal, 1987).
Immunologic reactivity is in turn regulated by sex [steroid] hormones.
This observation was initially made in a species of hybrid mice
(known as NZB/NZW) that spontaneously develops a syndrome
analogous to human SLE. De—sexing the mice exacerbates SLE in
pre—pubertal males but does not effect the disease course of females.
Administering androgens to females, however, results in a normal
life span and increases survival rates in mice already afflicted with
SLE (Talal, 1987).
12
The regulation of immune processes by sex hormones is only possible
if lymphocytes have androgen and oestrogen receptor sites. These
exist on T—lymphocyte suppressor cells found in the thymus gland.
Here both androgens and oestrogens decrease their reactivity.
Receptor sites also exist on suppressor cells in the spleen and lymph
organs. Here immunological reactivity is decreased by oestrogens and
increased by androgens. Sex hormones also regulate interleukin-2
levels and thus killer and suppressor cell activities. The functions of
interleukin-2 are diminished by oestrogens and increased by
androgens (Bhalla, 1989).
GENETIC
The inheritance of SLE is associated with the sixth chromosome of
human cells which contains a region that controls immunological
functioning. This area is generally known as the major
histocompatibility complex (MHC) and in humans as the human
leukocyte antigen (HLA) region. The HLA region has several
subregions that are genetically determined. In the autoimmune
disease rheumatoid arthritis (RA) for example, 75 percent of sufferers
inherit a subregion known as HLA—DRw4 and occasionally the
disease is associated with the DRw3 and DRw5 regions. Similar
studies with SLE patients have been less successful in identifying
associated HLA regions. DRw2 has been identified in 53.7 percent of
SLE patients and 26.1 percent of controls and Drw3 is reported in 45.1
and 20.4 percent of SLE and control subjects respectively (Blau &
Schultz, 1984).
13
VIRAL
Viral ribonucleic acid (RNA) from myoviruses and paramyxoviruses
have been consistently observed in SLE patients. High myoviruses
and paramyxoviruses levels do not, however, imply a viral etiology as
corticosteroid treatments suppress immune functioning making
patients more susceptible to secondary viral infections (Blau &
Schultz, 1984).
There remains, however, a general belief that viral agents are
somehow active in SLE (Talal, 1987). This stems from several
similarities between SLE and acquired immune deficiency syndrome
(AIDS). These include the production of antinuclear antibodies, lower
interleukin-2 levels, fewer natural killer cells, increase gamma
globulin levels and depressed B—lymphocyte suppressor cell
functioning.
TREATMENT
Despite the progress medicine has made toward understanding the
underlying symptomatology of SLE, practitioners remain
disadvantaged when treating patients (Decker, 1983). The etiology of
SLE is unknown and thus treatment can only focus on reducing
inflammation and treating symptoms as they arise, altering
medications as symptoms abate, intensify or change altogether (Blau
& Schultz, 1984). The treatment of SLE is, therefore, highly
individualistic.
14
PHARMACOLOGICAL
Prior to the 1940's no drug or class of drug was helpful in treating the
symptomatology of SLE. By the mid 1970's several classes of drug,
including antimalarials, corticosteroids, immunosuppressants and
non-corticosteroid anti-inflammatories had proved useful in
managing disease symptomatology (Hughes, 1988).
Antimalarials
Antimalarials came into use in SLE after their effectiveness against
discoid lupus erythematosus had been observed. Although the
mechanism of these drugs is unknown they inhibit antigen-antibody
(ANA) formation, reduce light filtration by the skin (about 30 percent
of disease sufferers exhibit photosensitivity) and inhibit viral
replication (viruses have been implicated in the etiology of SLE).
These drugs also reduce inflammation (Hughes, 1982). The most
widely used antimalarials are hydroxychloroquine (Plaquenil) and
mepacrine (Quinacrine).
There are, however, some side-effects that restrict the extensive use of
antimalarials. For example, there is a high incidence of
gastrointestinal disturbance, with nausea and vomiting, which is
associated with all antimalarials. Other side-effects include
premature greying of the hair, blotchy skin, convulsive seizures,
myopathy (muscle weakness) and skin rashes. The most serious
side-effects involve vision, usually blurring when the medication is
started and a 'halo' effect around bright lights. Furthermore, deposits
of these drugs collect in the cornea of the eye, causing tunnel vision
15
and possibly [irreversible] blindness (Hughes, 1982). Many of the
harmful side-effects from antimalarials are avoidable, through
careful monitoring and withdrawing the medication at the first signs
of side-effects. Additionally, regular visits to an optometrist can
reduce the incidence of visual impairments (Hughes, 1982).
Corticosteroids
Corticosteroids are the most widely used drug in the treatment of SLE.
While their mechanism is speculative, they are documented to
decrease T cell numbers, interleukin-2 levels and natural killer cell
activity (O'Leary, 1990). Like the antimalarials, however, there are
several side-effects from prolonged use or high doses of
corticosteroids. These include slowed hair growth, osteoporosis,
cataracts, decreased concentration span, heightened senses, masking of
infections, weight gain, elevated blood pressure, emotional problems,
psychosis and diabetes mellitus to name a few (Blau & Schultz, 1984;
Hughes, 1982; Sutton, Navarro & Stevens, 1984).
Immunosuppressants
Immunosuppressants directly suppress immune regulation via
decreasing lymphocyte production and interleukin levels. Their
side-effects include nausea and vomiting. Since
immunosuppressants suppress the immune functioning, they
increase the risk of secondary infections such as pneumonia.
Immunosuppressants also are known to interact with several
common drugs, including alcohol, aspirin and some tranquillisers to
cause other side-effects (Blau & Schultz, 1984).
16
Non-Corticosteroid Anti-Inflammatory Agents
Mild cases of SLE may be treated with aspirin (acetylsalicylic acid).
Aspirin contains an analgesic (pain reliever) and antipyretic (to reduce
fever) and effectively reduces inflammation and fevers associated
with SLE (Blau & Schultz, 1984). Side-effects from aspirin are often
less severe than those of the other medications mentioned above and
are often controllable. The risk of gastric side-effects, for example,
may be overcome by administering the drug along with buffer
solutions such as Alka-Seltzer (Hughes, 1982). There also are
stronger forms of aspirin designed to manage disease flares. These are,
however, used more cautiously as the risk of serious side-effects is
greater. Possible side-effects include allergies, liver complications,
intestinal bleeding and visual difficulties.
Summary
With the exception of non-corticosteroid anti-inflammatory agents
and low doses of corticosteriods, pharmacological treatments for SLE
can be aggressive and cause substantial side-effects. Since the
side-effects from medication can be more debilitating than the
symptom they treat, it is not uncommon for individuals to experience
considerable social and psychological problems.
PSYCHOLOGICAL
In Australia, self-help groups and Lupus Societies provide the major
sources of psychological management for individuals with SLE
(Hardy, 1985). Individuals also may receive private counselling or
psychological assessments as part of ongoing medical care.
17
Internationally there have been few published studies that evaluate
the efficacy of psychological interventions with SLE sufferers. This is
due to the limited understanding of how the disease effects the
psychological adjustment of sufferers. Investigations of the social and
psychological consequences of SLE would provide the foundations for
intervention studies.
MEDICAL ASPECTS AND PSYCHOLOGICAL ADJUSTMENT
The disease course of SLE may effect the social and psychological
adjustment of sufferers in a variety of ways. In about 15 percent of
sufferers, symptoms may directly cause psychopathology. For
example, hypertension can induce psychotic states. The waxing and
waning course of SLE may impede social and occupational
functioning and prolonged disease flares may erode social support and
self—efficacy beliefs. Symptoms that cause disfiguration such as facial
rashes may precipitate depressive states. Side—effects from treatment
such as weight gain also cause distress and corticosteroids can directly
precipitate depression. Finally, because it takes an average of three
years to diagnose SLE, individuals experience considerable stress in
not knowing what they are suffering (Hardy, 1985).
1.1.1 SUMMARY
This chapter provided a medical overview of SLE. The information
presented provides the foundations for understanding literature
reviewed in the next section. It also highlights the relationship
between medical factors, social and psychological adjustment. In
particular, symptomatology, diagnostic issues and treatment all can
18
contribute to social and psychological adjustment problems in
sufferers.
19
Chapter Two
Psychological Adjustment and Systemic Lupus Erythematosus
20
2.0.0 OVERVIEW
Chapter one established that immune system dysfunction is
responsible for the symptomatology of SLE, which in turn can cause
physical disability, psychosocial disruption and psychological distress
in sufferers. The next section reviews research on the psychological
and social factors related to SLE. In sections the review includes
studies with other chronic illnesses, as there was insufficient research
with SLE sufferers.
Consistent with other research, the chapter conceptualises factors
affecting chronic illness as either social, personal or disease outcome
measures (Hooker, Monahan, Shifren & Hutchinson, 1992; Revenson
& Majerovitz, 1991). Social resources are those variables influenced by
external events, they include stress, social support and social
networks. Personal resources are mediated by individuals' perceptions
and include self—efficacy and coping. Outcome measures are the
consequences of chronic illness and include physical disability,
psychosocial disruption and psychological distress (Husaini & von
Frank 1985).
2.1.0 SOCIAL RESOURCES
Stress, social support and social networks are important social
resources influencing illness outcome. This section reviews how
stress effects immune functioning, issues relevant to measurement
and the role of stress in SLE. The section then focuses on social
21
support and social networks, relevant measurement issues and how
they mediate disease outcome variables.
2.1.1 STRESS
A concise and informative definition of stress is provided by Cox
(1987).
"Stress, it is argued, can only be sensibly defined as a perceptual
phenomenon arising from a comparison between the demand
on a person and his ability to cope. An imbalance in this
mechanism, when coping is important, gives rise to the
experience of stress, and to stress response. The latter
represents attempts at coping with the source of stress. Coping
is both psychological (involving cognitive and behavioural
strategies) and physiological. If normal coping is ineffective,
stress is prolonged and abnormal responses may occur. The
occurrence of these, and prolonged exposure to stress per se,
may give rise to functional and structural damage. The
progress of these events is subject to great individual
variation."
(p. 25)
STRESS AND IMMUNE FUNCTIONING
Immune cells have receptors for stress related hormones such as,
beta-endorphins, enkephalins, corticosteroids and catecholamines
(Bhalla, 1989; O'Leary, 1990). These hormones affect immune
functioning in different ways. For example, beta-endorphins enhance
22
overall immune functioning, while enkephalins stimulate
T—lymphocyte and natural killer cell activity. Catecholamines
(epinephrine and norepinephrine) cause the release of lymphocytes
from storage and increase natural killer cell activity. Corticosteroids
reduce T—lymphocyte numbers, impair interleukin-2 production and
decrease natural killer cell activity.
Immune cells also manufacture hormones that influence CNS
functioning. For example, interleukin-1 and interleukin-2 act on the
hypothalamus and pituitary gland to raise adrenocorticotrophic
hormone levels. Other CNS hormones synthesised by immune cells
are substance P, beta—endorphins, enkephalins, corticosteroids and
catecholamines (O'Leary, 1990).
Another line of inquiry investigates the relationship between
exposure to acute or chronic stress and changes in immune
parameters. Immune system responsiveness to acute stress was
investigated by Zakowski and associates (Zakowski, McAllister, Deal &
Baum, 1992). Following a stressful film, lower lymphocyte numbers
were observed in 20 healthy men. This change was evident 15
minutes after stress exposure and lasted for about 90 minutes. A two
week follow—up, however, reported that temporary lymphocyte
alterations did not increase illness susceptibility.
Individuals exposed to chronic stressors, such as carers of Alzheimer's
disease patients, also have impaired immune functioning.
Kiecolt—Glaser and associates (Kiecolt—Glaser, Glaser, Shuttleworth,
23
Dyer, Ogrocki & Speicher, 1987) found care givers had lower
helper:suppressor cell ratios, T lymphocyte and T helper cell numbers
than the comparison group. Although differences between natural
killer cells and T suppressor cell numbers were not apparent, carers
had higher titers to Epstein—Barr virus suggesting poor immune
reactivity to antigens.
Since psychological variables can moderate stress responses, they also
should mediate immune functioning and subsequent disease
outcome. In one study, only individuals with low social support had
impaired immune functioning (Baron, Cutrona, Hicklin, Russell &
Lubaroff, 1990). This relationship was not mediated by either
depression or stressful life events. However, a suitable comparison
group was absent and social support levels were determined by a
median split of the sample. Median splits have been demonstrated to
confound social support with stress levels (see Thoits, 1985 for a
review).
Social support levels also can mediate changes in immune
functioning resulting from examination stress (Jemmont & Magloire,
1988). Salivary antibody (IgA) levels were assessed prior to, during and
post examination time in 15 university students. Antibody levels
were lowest during exam times and highest 14 days after exams
finished. Students with higher social support had the lowest IgA
levels and were in better health than the low support group. However
changes in diet and sleep typically accompany academic stress, so these
may have contributed to immune alterations (O'Leary, 1990).
24
Personal resources such as locus of control buffer the relationship
between daily hassles and immune functioning (Kubitz, Peavy &
Moore, 1986). Using a sample of individuals with either high or low
reported hassle levels, no significant differences in IgA titers were
evident. An internal locus of control, however, was associated with
lower IgA levels. This suggests it is perceived control that effects
immune functioning rather than stress. Nevertheless only one
percent of IgA protein becomes anti-body reactive upon encountering
an antigen making the index an unreliable assessment of immune
functioning (O'Leary, 1990).
Another personal resource, self-efficacy also mediates the relationship
between stress and immune functioning. Individuals provided with
training to enhance self-efficacy reported less stress and showed
increases in immune efficiency as measured by B-lymphocyte, T-cells
and interferon levels (Wiedenfeld, O'Leary, Bandura, Brown, Levine
& Raska, 1990). Although the study controlled for confounders of
immune functioning, such as diet, menstrual cycle and circadian
rhythms, its limitation was the exclusion of a suitable comparison
group (O'Leary, 1990).
The cited studies suggest the immune system is highly reactive to both
acute and chronic stress. They also suggest social resources (e.g., high
social support) and personal resources (e.g., self-efficacy and locus of
control) mediate the stress response and hence immune functioning.
Nevertheless, it remains to be demonstrated how short-term immune
alterations influence the disease process.
25
MEASUREMENT
The previous section discussed the relationship between stress and
immune functioning without regard to the controversy regarding
stress measurement. The next section distinguishes between the
different approaches and outlines the rationale for the measurement
strategy adopted in the present study.
There are three approaches to measuring stress. The first
conceptualises stress in terms of [physiological] responses such as heart
rate and blood pressure. Measuring the physiological concomitants of
stress arose from Selye's notion of a General Adaptation Syndrome
(GAS; Cox, 1987). The GAS has three stages. During the first stage the
body demonstrates changes characteristic of stress such as an
accelerated heart rate and increased blood pressure. This phase is
accompanied by decreased resistance to disease. In the second stage the
body adapts to prolonged stress and resistance to disease increases. The
final stage is characterised by exhaustion. In this stage the body's
resistance to disease decreases and if stress is prolonged the organism
becomes ill and may die.
Physiological response measures are not widely used in studies of
chronic illness as they confound disease symptomatology with signs of
stress. They also do not correlate with the three GAS stages, suggesting
other factors mediate stress responses (Cox, 1987).
The second approach measures stress as a stimulus. This model
assumes that external events have the potential to cause strain or
26
stress within a person. Stimulus models typically use either life event
or daily hassle inventories as stress measures. Life events are major
social changes that demand adaptation from an individual. Examples
include divorce, death of spouse and birth of a child. Hassles are
ongoing problems that cause social disruption. They include noisy
neighbours and work stress (Chamberlain & Zika, 1990). The life
events and daily hassle stress measures are the most popular
approaches in chronic illness research because they quantify stress and
are easily administered.
The final approach uses an interactional paradigm, assessing stress as a
stimulus and a response (Cox, 1987). Research adopting this approach
also measures variables that moderate the stress approach such as
self—efficacy and coping skills. The distinctions between the different
measurement approaches are however becoming less clear as
researchers routinely measure a range of behavioural and cognitive
factors that effect stress reactions. Whilst the stimulus approach is
adopted in the present study, it is considered in the wider context of
other cognitive and behavioural factors.
LIFE EVENTS AND DAILY HASSLES
Since the stimulus approach is less likely to confound disease
symptomatology with stress, it is used widely in chronic illness
studies. Two extensively used measures are life event and daily hassle
inventories. This section provides a description of each assessment
approach and a discussion of their relative merits.
27
LIFE EVENTS
These are assessed by assigning standardised weights for the amount of
readjustment a given event requires. The weights are summed to
yield an index of life change or stress. Higher life change scores are
associated with an increase in psychological distress, psychosocial
dysfunction and physical symptoms (see Felner, Farber & Primavera,
1983 for a review). Correlations between life change and disease are
however small, ranging from .10 to .20 (Felner, et al., 1983). This
suggests that other factors such as personal resources mitigate the
relationship between stress and disease (Feiner et al., 1983).
DAILY HASSLES
A similar methodology assesses daily hassles as antecedent to disease
outcomes. This approach has, however, notable differences to the life
event method. It does not assume standardised stress scores, rather
respondents estimate the amount of stress and pleasure (uplift) an
event provides (Chamberlain & Zika, 1990).
Studies measuring both life events and daily hassles suggest the latter
approach is a better predictor of disease outcome ( Weinberger, Hiner &
Tierney, 1987; Chamberlain & Zika, 1990). Daily hassles and uplifts
account for more variance in concurrent and subsequent disease
outcomes than do stressful life events. Daily hassle and uplift
inventories also have stronger test—retest reliabilities for the reported
number and rated severity of events, when compared with life event
inventories (Chamberlaine Sr Zika, 1990). For the aforementioned
28
reasons the daily hassle and uplifts approach was adopted in the
present study.
LIFE EVENTS, HASSLES AND SLE RESEARCH
Only a few studies document the impact of stress on SLE and they do
not typically measure variables mediating the stress/disease outcome
relationship. The earliest was concerned with the ways stress
contributed to the onset of SLE. Otto and Mackay (1967) defined stress
as "the conscious experience of tension— that is, depression,
frustration, anger or anxiety, or undue physical strain" (p.489).
Twenty SLE volunteers and a comparison group of women who had
an accidental haemorrhage during pregnancy were matched for age,
sex and socioeconomic status. Stressful life events were assessed via a
structured interview. Significantly more SLE (100%) than control
(60%) subjects reported that stress preceded the onset of their
condition. A further 65 percent of SLE patients reported that life
events also had preceded a disease exacerbation. The most frequently
reported life events involved interpersonal relationships for both SLE
and control subjects.
The Otto and Mackay study has several methodological problems that
detract from the value of its findings. The rater was not 'blind' to the
groups' diagnoses and individuals recalled stressful life events that
occurred as long as 15 years prior to disease onset. The average time
since diagnosis was 6.5 years for SLE sufferers and 3.5 years for controls
making the memory of the events surrounding illness onset more
29
reliable for the latter group. Finally, the researchers confound their
stress and disease outcome measures.
More recent research has focused on the notion that chronic illness
leads to elevated stress levels and this exacerbates disease flares. In one
study, 80 percent of SLE volunteers reported they felt stress preceded
disease flares and aggravated their illness (Laing, Rogers, Larson,
Eaton, Murawski, Taylor, Swafford & Schur, 1984). This relationship
was further investigated in a prospective study using life event
methodology (Rimon & Kronqvist, 1988). Over a 3.5 year period, 50
percent of SLE sufferers reported one or more stressful life events
preceded a disease flare. The most frequently reported events included
loss of a spouse, serious illness of a close family member, marital crisis
and financial difficulties. Although this study used a prospective
design, a comparison group was not included. Thus, it is unclear
whether life events occur more often in SLE patients than in the
general population. The study also did not include personal resource
measures such as self—efficacy and coping, to determine whether these
mitigate stress levels and hence disease outcomes.
Using a daily hassles measure, Wekking and associates ( Wekking,
Vingerhoets, van Dam, Nossent & Swaak, 1991) investigated whether
hassle levels were higher in SLE than RA sufferers. Whilst no
differences in stress levels were apparent, stress was related to physical
and psychosocial status for SLE but not RA sufferers. This study also
has significant methodological problems. For example, the sample
size was small and the assumptions of MANOVA were not met. The
30
effects of uplifts on well—being were not considered. A fatigue or
boredom effect also was present, as subjects failed to complete the
measures across consecutive assessment occasions. Furthermore,
inclusion of a healthy control group would have allowed conclusions
regarding whether a diagnosis SLE or RA in itself, leads to elevated
hassle levels.
Given the methodological problems of the studies cited above, it
remains to be established whether individuals with SLE experience
greater stress levels than other chronically ill people or the general
population. How social and personal resource variables mitigate the
stress disease relationship also has not been reported. The present
study adopts the daily hassle and uplift approach, to investigate group
differences in stress and whether these measures predict disease
outcomes.
SUMMARY
Immunological studies demonstrate hormonal links between the
immune and central nervous systems and psychological studies
suggest that immune changes coincide with both acute and chronic
stressors. Immune changes are however highly individualistic and
may either increase or decrease upon exposure to stress.
Measuring stress as a stimulus, the reviewed studies suggest life
events and daily hassles precede the onset of SLE and subsequent
disease flares. These findings are however unimpressive when their
methodological limitations are considered— most are retrospective,
31
uncontrolled or include only one comparison group. A two
comparison group design is necessary for determining whether high
stress levels are specific to SLE. There also is a need to investigate if
stress predicts disease outcome when other social and personal
resources are incorporated into the model.
2.1.2 SOCIAL NETWORKS AND SOCIAL SUPPORT
Research has differentiated social networks from the functions of
social support, though the terms are often used interchangeably.
Social networks (or social embeddedness) can be divided into
structural and interactional parameters (Cohen & Wills, 1985).
Structural parameters include the number of network members and
embeddedness in social organisations. Interactional dimensions
include network composition (e.g., the relative number of friends,
co—workers or relatives) and contacts between network members.
Social (or functional) support refers to a more specific idea than
network. Its assessment involves identifying those aspects of social
relationships that promote psychological and physical well—being.
These include belonging, instrumental, self—esteem and informational
aid (Cohen Sr Wills, 1985). Belongingness (also known as diffuse
support and social companionship) is spending time with others in
recreational or leisure activities. This may reduce distress by, for
example, distracting individuals from worrying events or enhancing
feelings of affiliation. Instrumental (or material or tangible) aid
involves the provision of actions or materials, such as assistance with
32
work or providing money to pay bills. Receiving instrumental
support may reduce distress by allowing the individual more time for
other activities. Self—esteem (or emotional or expressive) support
refers to communications or demonstrations that a person is valued.
This promotes feelings of self—esteem and reduces vulnerability to
stress. Informational (or appraisal) assistance includes the provision
of advice and feed—back, that may aid in coping. It is likely that
information support reduces stress by helping individuals to
understand or define their problems.I
Since the distinction between social support and network has
important assessment implications and explains contrary research
findings, it is maintained throughout this text. The term 'social
relationships' will describe the characteristics of social networks and
support.
MODELS
Social relationships may influence health in a variety of ways. Social
resources may be mobilised only when an individual is, for example,
ill or under stress. This is the buffering model of support and is
shown statistically whenever an interaction between illness [or stress]
and support is •found (Cohen & Wills, 1985; Thoits, 1982). The
peripheral model of support is a variant of the buffering hypothesis
(Henderson, 1984; Cohen & Wills, 1985). It asserts that support
influences health by helping with the recovery from an event after it
' Although topologies distinguish support functions, research suggests they correlate (Cohen, Mermelstein, Kamarck & Hoberman, 1985).
33
has occurred. Evidence for the peripheral model also comes from a
statistical interaction between support and stress.
Social relationships also may have a beneficial effect irrespective of
whether an individual is ill or experiencing a stressful event.
Evidence for this model comes from a statistical main-effect for
support without the presence of an interaction effect (Cohen & Wills,
1985; Thoits, 1985). There is research to support both the main and
buffering models and they are not mutually exclusive (Cohen & Wills,
1985).
THE LINK BETWEEN SOCIAL RELATIONSHIPS AND DISEASE OUTCOMES Whether social relationships have a main- or buffering-effect, they
protect individuals from stress and reduce the risk of physical and
psychological ill health (Wallston, Alagna, DeVillis & DeVillis, 1983;
Cohen & Wills, 1985) How social relationships influence health
requires clarification. Proposed mechanisms include promoting
healthy life styles, coping assistance and influencing physiological
processes and therefore possibly disease outcomes.
SOCIAL NETWORKS
Social networks promote generalised feelings of psychological
well-being that protect individuals from ill health. They provide
members with a sense of predictability and stability, norms for
behaviour, encourage positive affect and enhance feelings of
self-worth and belonging (Cohen & Wills, 1985). Establishing and
34
maintaining social network ties is mediated by personal resources such
as self-efficacy and the personality dispositions of network members
(Monroe & Steiner, 1986).
SOCIAL SUPPORT
Social support may influence disease outcomes by promoting 'coping
assistance' (Thoits, 1986). Support functions help distressed
individuals to cope by reinforcing their efforts to change the meaning,
feelings, or management of stressful circumstances. Tentative
evidence for this hypothesis comes from the noted similarities
between topologies of coping and support. For example,
problem-focused coping and instrumental support, both consist of
attempts to remove or alter threatening environmental circumstances.
Similarly, emotion-focused coping and emotional support, attempt to
alter negative feelings that accompany distress.
Social support also may influence physiological reactions to stress. For
example, one study measured support as a coping strategy and found it
predicted 33 percent of natural killer cell activity (Levy, Herberman,
Whiteside, Sanzo, Lee & Kirkwood, 1990). A study with Japanese
living in Hawaii found low social support levels predicted high blood
pressure independently of other risk factors such as smoking and
alcohol consumption (Joseph, 1981 in Berkman, 1984). Social support
also may moderate health related behaviours such as seeking medical
advice, smoking, alcohol consumption and blood pressure (Levy et al.,
1990). Finally, social support promotes adherence to complicated
35
medical regimes and life style changes (Gottielb & Green 1984;
Zimmerman & Connor, 1989).
• MEASUREMENT ISSUES
Social network measures can be divided into specific and global
indices. Specific assessments ask about a single parameter of network
structure, such as the number of significant others who potentially
provide social support. Global measures simultaneously index
connections with, for example, friends, neighbours and community
organisations (Cohen & Wills, 1985). Network size is a better predictor
of the main—effect model than are global measures (Cohen & Wills,
1985; Heitzmann & Kaplan, 1988).
Social support measures also can be distinguished along the
global/specific dimension. Global measures ask about several
dimensions of social support such as emotional, informational and
instrumental aid. Specific measures ask about one functional aspect of
social support, such as the context in which emotional support was
received .2
Global social support measures usually yield support for the buffering
model (Cohen & Wills, 1985). Specific measures only show a
buffering effect if they coincide with support requirements. For
example, instrumental support relieves financial stress.
2 This is also known as enacted support (Barrea, 1986)
36
Based on empirical findings (see Heitzmann & Kaplan, 1988 for a
review), the present study uses a specific social network measure to
investigate whether individuals with SLE have adequate access to
potential sources of social support. A global measure of social support
is also included to determine whether SLE sufferers have levels of
functional support comparable to healthy and other chronically ill
people. The main- and buffering- effect models are not investigated,
as longitudinal data that control for pre-existing social support and
stress levels are required (Thoits, 1985; Cohen & Wills, 1985).
SOCIAL RELATIONSHIPS AND AUTOIMMUNE DISEASE RESEARCH Since the role of social relationships in the outcome of SLE has not
been reported, the following discussion reviews recent research with
other autoimmune diseases. Although depression is the outcome
measured in most studies, several also consider disability and pain
measures.
A study of multiple sclerosis (MS) sufferers found individuals with a
progressive condition had larger social networks than persons with a
relapsing-remitting disease course (Wineman, 1990). This finding
suggests network size grows as disability levels increase and
individuals rely on significant others for self-care. Whether social
network members were potential sources of social support also was
investigated. Perceived unsupportiveness from network members
predicted depression in individuals with a progressive disease course.
This finding was independent of demographic factors such as age, sex
and socioeconomic status. Since the Wineman study was
37
cross—sectional, the possibility that depression limited access to social
network members cannot be excluded.
The efficacy of the buffering and main effect models was examined
prospectively by Brown and associates (Brown, Wallston & Nicassio,
1989). Rheumatoid arthritis sufferers completed questionnaires asking
about emotional support, network size, depression, disability and pain
on three assessment occasions spanning 18 months. Low levels of
emotional support, but not the number of network members, were
associated with elevated depression scores. This relationship was
independent of pain severity, disability and demographic factors such
as age and education level. Emotional support also interacted with
pain severity. Individuals with high pain and low social support were
more depressed than people with high social support and pain levels.
This interaction was only present in a cross—sectional analysis of the
data and not longitudinally. Furthermore, a path analysis of the data
suggested that low social support levels resulted in depression which
in turn decreased social support levels. This latter finding
demonstrates how depression can confound social support levels.
Another study with 149 RA sufferers found that baseline social support
levels predicted the severity of depression 15 months later (Fitzpatrick,
Newman, Archer & Shipley, 1991). This finding was independent of
initial depression and social support levels. This study used The
Interview Schedule for Social Interaction which confounds network
size with functional support, so it is not clear whether social
relationship have a main or buffering effect.
38
A different research strategy looks at the positive and negative effects
of social relationships (Revenson, Schiaffino, Majerovitz & Gibofsky,
1991). Revenson et al. found positive support exchanges predicted
lower depression levels, while negative exchanges predicted high
depression levels. The interaction between support and depression
levels suggested that the positive aspects of support were not cancelled
out by negative transactions. The highest depression levels were
apparent in RA sufferers with high number of negative transactions
and few positive social supports. A limitation of the Revenson et al.
study is stress was not considered as covariate of social support
satisfaction.
Social support and social networks can influence disease outcomes in
individuals with MS and RA. This occurs through embeddedness in
social networks and through the functional aspects of social support. It
also appears that only positive social support exchanges are beneficial
to psychological well—being. How personal resources, such as
self—efficacy and coping strategies, interact with social support to
predict disease outcomes has not been reported.
SUMMARY
Studies suggest that high levels of social support protect chronically ill
individuals from depression, disability and pain. Because these
studies use.correlational designs, it is not clear whether social support
and social networks are similar in chronically ill individuals and
healthy controls. This question is fundamental to SLE research, as
there have been no published studies on social support and networks
39
of sufferers. How social networks and support interact with personal
resources also is unclear. For example, individuals with high
self-efficacy may better mobilise support networks and thus minimise
the impact of stress on disease outcome.
2.2.0 PERSONAL RESOURCES
Personal resources are those variables that are influenced by
perceptions, they include self-efficacy and coping strategies. The next
section reviews Bandura's notion of self-efficacy and the factors that
promote efficacy beliefs. The limitations of self-efficacy theory are
considered and a wider definition of the construct adopted. The
operationalisation of self-efficacy is discussed, as well as how it differs
from related personal resources. Finally, how self-efficacy interacts
with autoimmune diseases such as SLE is considered. The second part
reviews the Lazarus and Folkman (1984) coping model and those
studies investigating coping in autoimmune diseases.
2.2.1 SELF-EFFICACY
Bandura and associates (Bandura, O'Leary, Taylor, Gauthier & Gossard,
1987; Bandura, Cioffi, Taylor, Brouillard, 1988) assert both efficacy and
outcome expectations mediate aspects of health behaviour.
Self-efficacy expectations are individuals' beliefs about their capability
of performing a specific behaviour in a given situation (Bandura,
1977). Outcome expectations are individuals' estimates that a given
behaviour will lead to a specific outcome. The distinction between
efficacy and outcome expectation can be clarified using an example.
40
Individuals may be sure that a particular slimming plan will reduce
weight (outcome expectancy) but lack the confidence they can
persevere with the diet (self—efficacy).
Integral to self—efficacy theory is the concept that expectations vary on
magnitude, strength and generality (Bandura, 1977). Magnitude refers
to the ordering of tasks by difficulty level. Given a hierarchy of tasks,
persons with low magnitude expectations can perform only the
simpler tasks. While individuals with high expectations feel they can
complete most tasks. Strength is an individual's probability estimate
of completing a task. Generality is the extent to which efficacy
expectations generalise beyond a particular situation to other
situations. For example, abstinence from alcohol achieved as an
inpatient may not continue upon release from hospital.
Efficacy expectations develop from performance accomplishments,
vicarious experiences, verbal persuasion and emotional arousal
(Bandura, 1977). Most important for the development of efficacy
expectations are performance accomplishment or learning from
personal experience. Mastery of a difficult or feared task not only
increases efficacy expectations, but also promotes skills for coping with
problematic situations. Vicarious experiences are derived from the
observations of other's successes and failures on a task and is
analogous to behavioural modelling. To observe an individual
successfully complete a task does not, however, ensure personal
success on one's first or later attempts at the same task. For these
reasons, vicarious experiences are less important to the development
41
of efficacy expectations than performance accomplishments. In verbal
persuasion individuals are instructed that they can master a task.
Since success or failure has not been personally experienced, verbal
persuasion contributes only moderately to the formation of efficacy
expectations. The final source of efficacy information comes from
emotional arousal. Stressful situations can cause anxiety and
depression that may impede an individuals task performance and
lower efficacy expectations.
THEORY REFINEMENTS
It seems appropriate to modify self-efficacy theory given recent
empirical findings. Bandura (1978) maintains it is the expectation that
behaviour cannot be sustained that mediates task performance.
Overwhelming evidence suggests, however, that it is outcome
expectations that mediate self-efficacy beliefs (e.g., Maddux, Sherer &
Rogers, 1982; Marzillier & Eastman, 1984; Wang & Richarde, 1988).
This can be illustrated by a hypothetical situation requiring a
non-phobic individual to perform two identical tasks involving
picking up a snake. In one task the snake is harmless and in the other
poisonous. It is likely that self-efficacy beliefs will differ for the tasks
(higher for the harmless than the poisonous snake) and these
variations arise from the different outcome expectations.
The predictive validity of self-efficacy expectations also have been
questioned. Investigations consistently demonstrate that past conduct
predicts future behaviour more accurately than self-efficacy
expectations (e.g., DiClemente Prochaska & Gibertini, 1985; Godding &
42
Glasgow, 1985), though this varies across different individuals and
situations (Garcia, Schmitz & Doerfler, 1990). In fact, when past
behaviour is statistically controlled the association between efficacy
and future behaviour is not statistically significant (Garcia et al., 1990).
Although Bandura (1978) acknowledges dispositional influences,
situational factors are considered the primary mediators of
self—efficacy. Empirical research suggests, however, that both
dispositional and situational factors mediate self—efficacy expectations.
When a situation is ambiguous, dispositional self—efficacy expectations
are the best predictors of performance. If circumstances are clearly
defined then task—specific ratings best predict behaviour ( Wang &
Richarde, 1988).
Psychometric difficulties also pervade the assessment of self—efficacy.
The validity of self—efficacy ratings comes from their correlation with
performance measures (Bandura, 1982). This logic has several
problems. Ratings may be reactive due to the close temporal proximity
of self—efficacy and performance assessments. The identical nature of
efficacy and performance tasks also may lead to measurement
redundancy. Finally, the high correlations between efficacy and
performance assessments may be mediated by other factors such as
self—esteem (Kazdin, 1978).
Self—efficacy theory requires some conceptual revisions, given its
theoretical and methodological limitations. Self—efficacy is a cognitive
construct influenced by outcome expectations and individuals'
previous performance accomplishments. In new situations
43
dispositional self-efficacy expectations influence performance. The
resulting outcome may modify dispositional efficacy expectations and
allow individuals to predict their performance on subsequent [similar]
tasks.
The aforementioned empirical modifications to self-efficacy theory
have measurement implications. Since efficacy and outcome
expectancies are highly correlated, this eliminates the need for separate
assessments. In addition, dispositional measures predict a wider range
of behavioural outcomes and allow comparisons between studies. The
present study uses a dispositional measure for assessing whether SLE
sufferers have lower self-efficacy and outcome expectations.
RELATIONSHIP TO OTHER PERSONAL RESOURCES
The concise operationalisation and measurement of self-efficacy
depends on conceptual clarity. It is, therefore, necessary to distinguish
self-efficacy from related personal resources. Health locus of control
refers to individuals' attributions of whether their health is controlled
by internal or external factors, whereas self-efficacy pertains to
behavioural expectations ( Wallston, Wallston, Smith & Dobbins,
1987). Internally oriented individuals have generalised expectations
that their health is dependent on personal behaviour. Externally
directed persons believe illnesses are unrelated to personal behaviour.
Locus of control can interact with self-efficacy in different ways
(Strecher, DevIllis, Becker & Rosenstock, 1986). In a situation where
control is possible, a person with high self-efficacy expectations copes
with distress. If a highly efficacious person is denied control or coping
44
efforts continue in situations where control is not possible, then
distress results. Individuals with low self—efficacy who are given
control do not cope with stressful conditions. If low efficacious
individuals are denied control over stressful events then distress may
be minimised. These predictions are supported by empirical evidence
(see Litt, 1988 for a review) and have implications for the interaction of
self—efficacy with coping behaviour.
Attribution styles differ from self—efficacy beliefs, in that the former
pertain to the causes of events and not behavioural expectations. If,
for example, illness is attributed to external, specific and unstable
circumstances coping will be satisfactory and distress minimal. If,
however, illness is attributed to internal, global and stable factors
coping will be less effective and depression may arise (Litt, 1988).
Self—esteem refers to individuals liking or respect for themselves,
whereas self—efficacy pertains to performance capabilities (Litt, 1988).
This distinction can be illustrated by an example. An individual can
have high self—efficacy for completing a task but derive no increase in
self—esteem from its successful accomplishment. Frequently, however,
high self—efficacy and self—esteem occur together. That is, individuals
develop high self—efficacy from activities that also promote
self—esteem.
The coping process involves primary and secondary appraisals
(Larazus & Folkman, 1984). Primary appraisals involve judgments of
whether an event is stressful and secondary appraisals concern
45
possible courses of action. Secondary appraisals are complex and
involve decisions about possible coping strategies, the likelihood of
their success (outcome expectation) and whether the individual can
apply these strategies (self—efficacy). Efficacy expectations are part of
the secondary appraisal process (Strecher et al., 1986). Efficacy beliefs
also are mediators of the duration and effort of coping behaviour
(Bandura, 1977, 1978, 1982). Highly efficacious individuals use a wider
variety of strategies to cope with the temptation to smoke than persons
with low self—efficacy beliefs (Garcia et al., 1990). High self—efficacy
expectations also are associated with adaptive problem—focused coping
and low expectations with the use of less effective means of reducing
distress, such as emotion—focused coping (DiClemente, et al.,1985).
The personal resources discussed above interact with self—efficacy
beliefs to influence behaviour. For example, high self—esteem and
self—efficacy beliefs usually co—occur. There are, however, clear
distinctions between the reviewed personal resources and self—efficacy.
These distinctions were emphasised to affirm that the present study is
focusing on the specific concept of self—efficacy and not a wider
definition adopted in some research.
SELF—EFFICACY AND AUTOIMMUNE DISEASE RESEARCH
Studies with chronically ill individuals usually adopt wide definitions
• that only remotely resemble Bandura's notion of self—efficacy. The
following review considers only studies that narrowly define
46
Bandura's notion of self-efficacy. These studies have used either RA
or SLE sufferers.
A study of 101 individuals with rheumatoid arthritis found high
self-efficacy scores were related to less functional disability
cross-sectionally and prospectively after one year (Schiaffino,
Revenson & Gibofsky, 1991). Strong self-efficacy beliefs also were
related to the use of adaptive problem-focused coping and lower
disability levels one year after the initial assessment. Self-efficacy was
not related to depression on either assessment occasion. Pain levels
did, however, interact with self-efficacy beliefs for predicting
depression after one year. When pain was minimal, self-efficacy was
not associated with depression; high pain levels accompanied by
strong self-efficacy beliefs were related to elevated depression levels.
Whether this latter finding was further mediated by problem-focused
coping skills was not considered. While the Schiaffino et al. study
demonstrates a complex interaction between self-efficacy and health, it
is flawed by the assessment strategies used. The self-efficacy measure
was specifically related to disability and thus not appropriate for
predicting depression, coping or pain levels.
A complex relationship between self-efficacy and life satisfaction is
also evident in the adjustment to rheumatoid arthritis (Smith,
Dobbins SE Wallston, 1991). Using path analysis the study found an
internal locus of control was associated with high self-efficacy and
greater life satisfaction, whereas the unavailability of instrumental
social support was associated with low self-efficacy and high
47
depression levels. High life satisfaction levels were predicted by high
self-efficacy beliefs, an internal locus of control and satisfactory
instrumental social support.
An intervention study found that enhancing self-efficacy levels lead
to changes in a range of cognitive and behavioural domains for
rheumatoid arthritis sufferers (O'Leary, Shoor, Long & Holman, 1988).
Enhancing self-efficacy beliefs decreased pain, disability, stress and
depression levels and increased physical functioning. High
self-efficacy levels also were associated with higher
suppressor /cytotoxic T-cell numbers. Strengthening self-efficacy
beliefs did not, however, enhance activity levels or improve
immunological functioning. This latter finding may have been due to
the confounding effects of medication on immune parameters.
Another limitation was that conservative statistical approaches were
not utilised in analyses- one-tailed significance tests were adopted and
Bonferroni corrections for multiple comparisons were not considered.
Thus it is difficult to conclude that increasing self-efficacy improves
cognitive and behavioural functioning in individuals with
rheumatoid arthritis.
A descriptive study with 201 SLE sufferers reported increases in
self-efficacy over time (Braden, 1991). Since there were no
experimental manipulations and no comparison groups were
included, Braden's data only provides test-retest reliability of
self-efficacy measure. Furthermore, the self-efficacy assessment used
a visual analogue scale in which respondents were asked "How
48
satisfied are you with your ability to control fatigue" (Braden, 1991,
p.162, italic added). No evidence of the construct validity of this
measure was provided.
In summary, self—efficacy beliefs concern one's capability of
performing specific behaviours. These beliefs arise from past
behavioural accomplishments and the expected outcome of a
situation. Empirical data suggest that self—efficacy mediates disease
outcomes, such as depression, disability and pain, in individuals with
autoimmune diseases. These studies have not, however, established
whether self—efficacy levels differ between chronically ill and healthy
people or whether self—efficacy is a significant predictor of disease
outcome.
2.2.2 COPING
The most widely accepted model of coping behaviour involves three
stages; stress appraisal, perceptions of control and coping behaviour.
While this model is well researched in psychology, it is less often
adopted by medical researchers. This section reviews the Lazarus and
Folkman (1984) coping model and reviews studies investigating
coping in autoimmune diseases. The review does not include studies
with SLE sufferers, as the author was unable to locate any published
studies.
THEORY
Lazarus and Folkman (1984) define coping as
"...the person's constantly changing cognitive and behavioural
49
efforts to manage specific external and/or internal demands
that are appraised as taxing or exceeding the person's
resources."
(p.141)
This definition asserts that coping efforts are dynamic, have cognitive
and behavioural properties and are a response to a taxing situation.
The Lazarus and Folkman coping model proposes that distress results
from how an individual appraises a stressful situation. The appraisal
process has three stages. The first stage is primary appraisal and
concerns judgments about whether an event is harmful. The next
stage is termed secondary appraisal and is concerned with whether an
individual perceives an event as controllable. In the third stage
individuals employ emotional and behavioural strategies that
alleviate stress.
Lazarus and Folkman also distinguish between problem and
emotion-focused coping. Problem-focused coping consists of
strategies aimed at problem solving or doing something to alter the
source of stress. Emotion-focused coping is aimed at reducing or
managing the emotional distress associated with a stressful event.
While most stressors elicit both problem and emotional focused
coping responses, problem-focused coping predominates when
individuals feel they can actively reduce stress and emotional focused
coping dominates when individuals believe that the stressor can only
be endured. Other dimensions of coping such as maladaptive coping
50
and social support as coping assistance also have been identified
(Thoits, 1986; Carver, Scheier & Weintraub, 1989).
The final assertion of the Lazarus and Folkman model is that coping is
a dynamic process that reflects the contextual aspects of stress. While
this notion has merit, coping also has dispositional qualities (Carver et
al., 1989). That is, individuals have a preferred set of coping responses
that they take into stressful situations. This study adopts a
questionnaire measuring both the contextual and dispositional aspects
of coping behaviour.
COPING AND AUTOIMMUNE DISEASE RESEARCH
Studies have focused on issues such as coping typologies, the use of
downward comparisons as a coping strategy and the relationship of
coping to depression, disability and pain. This section focuses on
studies of individuals with rheumatoid arthritis, as there has been no
research with SLE sufferers. Most of the cited research does not
incorporate current theoretical notions of coping and is not theory
driven.
A study with 158 outpatient RA sufferers used cluster analysis to group
individuals according to the coping strategies they most typically used
(Newman, Fitzpatrick, Lamb & Shipley, 1990). The mostly widely
used strategy was passive coping. Passive copers did not adhere to any
particular strategies but used a wide range of responses to a moderate
extent. Another group used both emotion and problem-focused
strategies to cope with their RA and associated pain. The third group
51
were active in coping with their condition. They rarely used social
support as coping assistance. The final group consisted of RA sufferers
who utilised social support or religion to cope with their condition.
These empirically derived groups were not distinguishable on
demographic factors, psychopathology, social support or disease
activity. Notable differences in disability scores were, however,
apparent between the groups, with active coping group reporting
lowest levels. While the results of this study are encouraging, the
measure of coping was devised on an ad hoc basis from existing scales
and its reliability was not established.
Another study examined downward and upward comparisons as a
coping mechanism in individuals with RA and mothers of acutely ill
newborn babies (Affleck, Tennan, Pfeiffer, Fifield & Rowe, 1987).
Downward comparisons involve viewing others as less fortunate than
oneself and upward comparisons concern viewing others more
favourably than oneself. The notion that downward comparisons are
common in RA and mothers was supported. Only rarely were upward
comparisons made. The majority of respondents, however, did not
use either downward or upward comparisons as a coping strategy. The
descriptive nature of this study and the fact that raters were not blind
to the hypotheses make the results unreliable.
The Coping Strategies Questionnaire (CSQ) conceptualises coping as
either cognitive or behavioural (Beckham, Keefe, Caldwell &
Roodman, 1991). Using this questionnaire Beckham and associates
found that RA sufferers using pain control and rational thinking as
52
coping strategies reported less depression, disability, hassles and pain
than individuals not using such strategies. This relationship was
independent of demographic factors including age and gender and
medical variables such as disease severity. Since this study used a
correlational design, the direction of the coping and adjustment
relationship cannot be inferred. Furthermore, the cognitive coping
dimension of the CSQ confounds personal resources, such as
self-efficacy and self-esteem, with the process of coping.
The relationship between coping strategies, pain and depression was
investigated by Brown and associates (Brown, Nicassio & Wallston,
1989). The subjects were 287 R A sufferers who had been diagnosed for
seven years or less. Two dimensions of coping were examined, passive
(or emotion-focused coping) and active coping (or problem-focused
coping). Cross-sectionally and over a six month period, an interaction
between passive coping, pain and depression was present. Individuals
who were passive copers with high pain levels were more depressed
than people not using such coping strategies. Individuals who were
active copers reported low depression and pain levels when compared
with passive copers. Since a correlational design was utilised, causality
problems also exist with this study. While passive coping in the
presence of pain may lead to high depression levels, depression may
lead to poor coping and elevated pain levels. There also was a
problem with the coping measure use in the Brown et al. study. The
range of scores for passive coping was greater than for active coping,
potentially biasing the assessment of the former coping dimension.
53
Furthermore, without the inclusion of a depressed pain comparison
group, few conclusions about result specificity are possible.
A longitudinal study with 45 RA sufferers used the Ways of Coping
Questionnaire (Lazarus & Folkman, 1984), to assess its relationship
with self-efficacy, disability and affect (Revenson & Felton, 1989).
More individuals relied on emotion-focused coping than on
problem-focused strategies. While coping was not associated with
either disability, self-efficacy or negative affect, it was associated with
positive affect. Individuals using problem-focused strategies were
more likely to report positive than negative affective states. Like the
aforementioned studies, the correlational design lead to cause and
effect problems. Also the effects of time-1 affect, disability and
self-efficacy were not partialled out when predicting time-2 coping,
thus confounding existing adjustment with subsequent coping
strategies.
While this review is not comprehensive, it highlights the limitations
of studies of coping in chronic illness sufferers. Most studies use
questionnaires without established psychometric properties, instead
choosing to derive coping measures ad hoc. Furthermore, few
investigations assess whether there are characteristic differences in
coping responses between different types of illnesses and whether ill
individuals cope differently from healthy controls.
In sum, the Lazarus and Folkman coping model is widely cited in
psychological research but rarely is incorporated in studies with
54
chronically ill people. The model proposes that coping occurs as a
three stage process and distinguishes between emotional— (passive)
and problem—focused (active) coping strategies. Although coping is
hypothesised as situation specific, it also has dispositional elements.
How individuals with SLE cope compared with other chronically ill
and healthy people has not been reported nor has the interaction of
coping with disease outcome measures.
2.3.0 DISEASE OUTCOME MEASURES
These measure the consequences of chronic illness and include
psychological distress (or psychopathology), physical disability,
psychosocial disruption (e.g., communication limitations) and life
style disruption (e.g., eating difficulties and recreational restrictions).
However, only one SLE disease outcome measure, psychopathology,
has received substantial research. The effects of SLE on the other
outcome measures has not been reported.
2.3.1 PSYCHOLOGICAL DISTRESS
High psychopathology (or psychological distress) rates have been well
documented in SLE sufferers and can be arbitrarily classified as either
organic or adjustment syndromes. Organic or neurological syndromes
arise from the pathogensis of SLE and include seizures and cognitive
decline. Adjustment reactions emanate from problems associated
with living with SLE. For example, the unpredictable disease course
may result in depression, fatigue may lower sufferers resistances to
stress and weight gains associated with using corticosteriods may lower
self—esteem.
55
INCIDENCE AND SYNDROMES
A study by Rimon, Kronqvist and Helve (1988) found a
psychopathology rate of 19 percent. The most common syndrome was
depression in 13 percent of SLE patients. Depressive symptoms ranged
from mild to severe cases, with neurotic depression most frequently
diagnosed. Organic brain syndromes were present in 10 percent of
individuals. The psychiatric status of 83 percent of the original sample
was followed longitudinally for three years. Over this period, 36
percent of individuals with SLE experienced depressive illness and 16
percent organic brain syndromes. These syndromes persisted during
the entire follow-up period. Although the Rimon and associates'
study is prospective, psychiatrists were not 'blind' to patients' previous
psychiatric histories and a comparison group was not included.
An investigation of psychopathology rates prior to and after the onset
of SLE as well as cross-sectionally during an interview shows the latter
approach yields the highest estimates (Lim, Ron, Ormerod, David,
Miller, Logsdail, Walport & Harding, 1988). The sample consisted of 40
sufferers (36 outpatients and 4 inpatients) and a comparison group of
14 R A sufferers and 13 inflammatory bowel patients. Six SLE and no
control patients reported signs of psychopathology before the onset of
their condition. Using DSM-III criteria, three SLE patients experienced
anxiety conditions, two major depressive disorder and one an organic
brain syndrome. Twenty-five SLE patients and eight controls reported
psychopathology after the onset of their condition. For individuals
with SLE, major depression was present in 16 instances, anxiety in four
cases and atypical psychoses in five individuals. At a cross-sectional
56
interview 40 percent of SLE and 30 percent of controls were identified
as 'psychiatric cases'. From the interview, two SLE patients had
psychotic symptoms, eight had major depression and six anxiety
disorders. Concurrent measures indicated that psychopathology was
associated with high stress levels, but not with objective indices of
disease activity. Furthermore, psychopathology was not associated
with the presence of neurological changes.
Psychiatric interviews and psychometric tests were used to quantify
psychopathology rates in 30 outpatients and 49 inpatients with a
diagnosis of SLE (Kremer, Rynes, Bartholomew, Rodichok, Pe1ton,
Block, Tassinari & Silver, 1981). Forty—six percent of the sample were
judged to have some current psychopathology, though the degree of
disturbance was only mild. A sample of 37 individuals completed the
MMPI, of this group 61 percent were classified as showing
psychopathology. Scores were elevated on the hypochondriasis,
depression and hysteria scales, a profile that is usually associated with
neurotic concerns. These findings were unrelated to disease severity,
neurological involvement or corticosteroid dosages. The efficacy of
psychiatric interviews and psychological testing cannot, however, be
evaluated as only a subsample completed the MMPI.
Elevated depression, hypochondriasis and hysteria scores on the MMPI
also were found by Liang and associates (Liang et al., 1984). This profile
pattern was unrelated to disease duration, stressful life event scores or
whether individuals were diagnosed with SLE or RA. For individuals
57
with SLE, however, depression was correlated with high social
disruption scores on the life events inventory.
Standardised psychological tests also were employed by Allen and
Glicksman (1986) to assess psychopathology in SLE patients. This study
found similar Profile of Mood States (POMS; McNair, Lorr &
Doppleman, 1971) between individuals with SLE and the norms for
healthy subjects. These groups in turn were significantly different
from psychiatric patients who had elevated POMS profiles. One
explanation for the contrary findings of the Allen and Glicksman
study is they used a community sample of individuals with SLE while
other studies use outpatient or hospitalised sufferers. A more likely
explanation, however, concerns design flaws with the study. Only 22
percent of individuals approached volunteered for the study and no
attempt was made to confirm these people met the ARA criteria for
SLE. The POMS also is not considered a measure of psychopathology
but rather an assessment of affect (McNair et al., 1971). There also were
no appropriate control groups, rather SLE sufferers were compared
with POMS norms.
In sum, the psychopathology rate for SLE sufferers varies between 19
and 71 percent. This large discrepancy arises from measurement
strategies and the classification of psychological states.
ETIOLOGY
The preceding review suggested that for about 10 percent of sufferers
psychopathology has an organic etiology and in five percent of SLE
58
patients it arises from the side—effects of medication. Over 85 percent
of psychopathology is reactive and arises from factors that are not well
understood.
ORGANIC
Psychopathology can result from disease complications such as
hypertension and renal dysfunction. When this occurs, the
administration of corticosteroids reduces disease severity and
symptoms of psychopathology (Adelman, Saltiel & Klinenberg, 1986).
Changes in cerebral blood flow occasionally cause psychotic symptoms
in sufferers (Adelman, et al., 1986). Immune deposits in the choroid
plexus of the brain also are implicated in the etiology of psychotic
episodes. Similar deposits are reported in the brains of individuals
with schizophrenia, leading to the notion that SLE may provide a
model for schizophrenia. Autopsy studies report enlarged brain sulci
in individuals with a history of psychiatric symptoms, but these
observations are based on small samples and are not consistently
replicated (Adelman, et al., 1986). Fatigue also is a common symptom
of SLE and can lower depression and anxiety thresholds.
Corticosteroid medications cause signs and symptoms of psychosis in
approximately five percent of individuals with SLE. Individuals with
preexisting psychopathology or organic brain diseases are at greater risk
for steroid induced psychosis than are people without such a history
( Wallace & Dubois, 1987). The notion of a steroid induced psychosis is
however controversial. Some evidence suggests that psychotic
symptoms can improve following administration of corticosteroids.
59
Furthermore, withdrawal of steroid does not always lead to the
symptoms of psychosis abating.
ADJUSTMENT REACTIONS
The majority of psychological syndromes are reactive and probably
result from changes in social functioning or the erosion of personal
resources. Limited research has documented that elevated stress levels
precede psychological distress and that self—efficacy training lowers
distress. Research with other autoimmune diseases suggests that
decreases in social support and emotion—focused coping strategies also
elevate psychological distress levels. Clearly further research on
variables moderating psychological distress is required.
2.3.2 FUNCTIONAL DISRUPTION MEASURES
Figure 1 provides a summary of the different approaches for assessing
health outcomes. Levels 1-4 are objective measures and are used
mainly in epidemiology studies to assess disease outcomes. Level one
assessments quantify self—reported symptoms of disease such as
headaches or somatic complaints. Level two measures the incidence
or prevalence of disease as an outcome. The third level is an indirect
disease outcome measure and is based on parameters such as
prescriptions or surgical procedures. Level five, estimates health
outcomes from mortality rates.
A different approach estimates functional disruption arising from
illness (level four). In this approach performance is classified as (1)
physical such as changes in ambulation, mobility and body movement
Psychological factors
60
Signs and Symptoms .l evel One)
Self-perceptions of illness
Medical diagnosis of disease • Level Two
ical treatrnent of disease Level Three
Mortality Level Five
Functional ci isahili ty , Psychological distress
Psychosocial disruption Level Foul
Figure 1: Medical approaches for assessing health outcomes (Modified from Bergner, 1988, page 82)
61
(2) psychosocial which includes disturbances in emotional behaviour,
communication and alertness behaviour and (3) life style covering
impairments in sleep, recreation, work and home management. The
correlation magnitude between objective (levels 1-3) and functional
approaches is typically moderate suggesting they measure distinctive
aspects of disease outcome. In behavioural research, however,
functional disruption measures have several advantages over the
objective approach. A range of medical complaints can be compared
irrespective of symptomatology or treatment. They also are sensitive
to improvements in patient activity levels and are easily administered
as self-report measures.
Only one study has measured the relationship between physical
disability, psychosocial impairment and stress in SLE sufferers
( Wekking et al., 1991). For individuals with SLE, but not the RA
group, high stress levels were associated with elevated physical
disability scores (i.e., mobility, physical ability, dexterity) and greater
psychosocial disruption (i.e., anxiety, depression and social interaction)
as assessed by The Arthritis Impact Measurement Scales (Meenan,
Gertman & Mason, 1980). Disease outcome measures also were
significantly correlated with objective indices such as auto anti-body
levels and erythrocyte sedimentation rate (an index of inflammation
and hence disease activity). Unfortunately, the study used a small
sample size (n=13) so the findings should be viewed with caution.
2.4.0 CHAPTER SUMMARY
Consistent with earlier studies, disease outcomes are postulated to be
62
influenced by social and personal resources. Social resources are those
variables influenced by external events and include stress, social
networks and social support. Personal resources are mediated by
perceptions rather than external events and include self—efficacy and
coping strategies. The outcome of chronic illness includes indices such
as psychological distress, physical disability or psychosocial disruption.
The social resources reviewed in this chapter were stress, social
networks and support. Stress levels were similar in SLE and RA
sufferers but higher than for 'healthy' controls ( Wekking et al., 1991;
Otto & Mackay, 1967; respectively). Furthermore, stress was related to
disease outcomes for SLE sufferers, but not for people with RA
( Wekking et al., 1991). Correlation research adds an additional
dimension to the comparative studies. One study found that stress
arising from a loss of social support exacerbated disease activity for SLE
sufferers (Laing et al., 1984). The aforementioned conclusions are
however based on a synopsis of findings from studies using different
respondents and methodologies. A more advantageous approach
would be to incorporate comparative and correlational designs to
investigate stress levels and disease outcomes in the same group of
subjects.
Comparative studies of social network size and support levels for SLE
sufferers are lacking. One correlational study reported that the loss of
social support in the presence of high stress exacerbated disease activity
(Laing et al., 1984). But the study did not test the buffering model of
social support. Correlational studies with other chronic conditions,
63
• however, generally do not find a main—effect for social networks
(Brown et al., 1989), but show a buffering effect for social support
(Brown, et al., 1989; Fitzpatrick et al., 1991; Revenson et al., 1991). Since
the affects of social relationships on disease outcome are not widely
reported for SLE sufferers, it would be advantageous to adopt both
comparative and correlational procedures to investigate these
hypotheses.
The personal resources reviewed in this chapter included self—efficacy
and coping. Comparative studies of self—efficacy have not been widely
reported for SLE or other chronic illness sufferers. Several
correlational studies have found that high self—efficacy perceptions are
associated with a large social network, more social support and the use
of problem—focused coping strategies (Wiedenfeld et al., 1990;
Schiaffino, 1991; Smith et al., 1991). Again, comparative and
correlational studies reporting the interaction of self—efficacy with
other social and personal resources, as well as how it relates to disease
outcomes are required.
Chronically ill people use more emotion—focused coping than
problem—focused strategies. Whether they differ from 'healthy'
controls has not however been reported. In correlational studies,
illness sufferers using more problem—focused coping strategies report
less disability and distress than those people who rely on
emotion—focused strategies. Furthermore, problem—focused copers
report fewer hassles and higher self—efficacy than people using
64
emotion—focused strategies (DiClemente, et al., 1985; Schiaffino, 1991;
Smith et al., 1991).
The disease outcomes reviewed in this chapter were psychological
distress, physical disability and psychosocial disruption. How social
and personal resources influence disease outcomes for SLE is not well
documented. For example, the incidence of psychopathology is widely
reported and is believed to stem from adjustment problems associated
with SLE. Nonetheless, how social and personal factors contribute to
psychological distress in SLE sufferers is not well documented. Using
physical disability as a disease outcome measure, one study found a
correlation with elevated stress levels in SLE sufferers ( Wekking et al.,
1991). Thus there also is a need for comparative studies to establish
where differences result on outcome measures and correlational
research to determine which social and psychological resources may
influence outcomes.
Throughout the chapter emphasis was placed on the need for
comparative and correlation studies. The present study, therefore,
includes another illness comparison group and healthy controls.
Multiple sclerosis (MS) was chosen as the other illness comparison
group for several reasons. It also is an autoimmune disease that
occurs more often in females than males and has its onset during the
child bearing years. The disease course of MS is characterised by flare
and remission periods and exacerbations are usually managed with
corticosteroids. Sufferers also are likely to experience their symptoms
several years before a diagnosis is reached. The important difference
65
from SLE, is that antibody attacks are specific to the myelin sheath
encasing central nervous system neurons. This difference in
symptomatology, rather than the demographic characteristics of the
diseases, will explain any observed disparities between the illness
groups. The inclusion of a healthy control group allows conclusions
about whether group differences are specific to chronic illness. The
three group comparative design makes a useful contribution to
research as it identifies and quantifies which social and personal
resources are adversely affected by having SLE. The design also allows
conclusions about whether changes are specific to SLE or occur in
other chronically ill people.
The study design also allows for correlational and regression analyses
to examine the relationship between variables cross-sectionally.
While these analyses will generate hypotheses for further research,
without longitudinal data firm conclusions about directionality and
causality are not possible. For example, decrements in the availability
of social and personal resources may result from, or contribute to,
disease exacerbation.
To conclude, the literature suggests a Disease Exacerbation Model for
the course of the disease and and its impact on social and personal
resources. This model predicts that the course of the chronic diseases
will lead not only to a deterioration in the disease outcome measures,
but also to a deterioration in various measures of social and personal
resources. It is also to be expected that there will be some underlying
casual relationships in which a diminution of certain social and
66
personal resources will impact upon the disease process further
exacerbating the outcome as indicated by the distress, disability and
disruption measures.
2.5.0 HYPOTHESES
GROUP DIFFERENCES
Following from the literature review, there is insufficient evidence to
predict differences between the SLE and MS groups on any social,
personal or disease outcome variable, except that the MS group may be
expected to report greater physical disability. In accordance with the
Disease Exacerbation Model, healthy controls may be expected to differ
from chronic illness sufferers on all the social, personal and disease
outcome measures. Expected differences between healthy controls and
the chronic illness groups are as follows:
a. The illness groups will report more hassles and fewer uplifts
than healthy controls.
The social network size of healthy controls will be larger when
compared with SLE and MS sufferers.
c. SLE and MS sufferers will report less social support when
compared with healthy controls.
d. Self-efficacy levels will be higher for healthy controls than the
chronic illness groups.
e. Controls will report more problem-focused coping than either
SLE or MS sufferers.
f. The chronic illness groups will report more emotion-focused
coping than healthy controls.
67
g. The chronic illness groups will report more psychological
distress than healthy controls.
h. The chronic illness groups will report more physical disability
than healthy controls.
i. The chronic illness groups will experience more psychosocial
disruption than healthy controls.
To assist in interpreting group differences, correlational analyses also
will be performed to identify relationships between personal, social
and outcomes measures. Stepwise regression will be used to
investigate the relative importance and strength of social and personal
resources in predicting disease outcomes.
68
Chapter Three
Method
69
3.1.0 DESIGN
The design of this study involved the comparison of three matched
groups: SLE, MS and healthy controls. The groups were matched for
age, gender, marital and socioeconomic status. The dependent
variables used in the study were measures of social resources,
personal resources and disease outcomes. Social resource measures
included hassles, uplifts, social networks and social support. Personal
resource measures were self—efficacy, problem— and emotion-focused
coping. Disease outcome measures were physical disability,
psychological distress and psychosocial disruption. A description of
the various measures and the psychometric properties is provided in
section 3.3.0.
The hypotheses were subsequently evaluated by analysis of variance
to assess differences in group means on the various dependent
variables. Correlation and regression analyses were also performed
to assess relationships between the social, personal and disease
outcome measures. For further details of the statistical procedures
see page 83.
3.2.0 PARTICIPANTS
The groups of participants were recruited in different ways. A
representative from the Tasmanian Lupus Society contacted
members to explain the study. Of the 50 members, 34 volunteered to
participate. This represents a response rate of 68 percent. The 34
70
volunteers met three or more ARA criteria and were diagnosed with
SLE by either a specialist rheumatologist or general practitioner.
For individuals with MS, a written explanation of the study was
forwarded by the Tasmanian Multiple Sclerosis Society only to
members with a diagnosis confirmed by a neurologist. This was
accompanied by a postcard asking about demographic information
and a reply paid envelope. Of the 280 members sent information
about the study, 141 volunteered to participate. This represents a
response rate of about 50 percent. Since it was not possible to
interview all the volunteers, a random sample of 40 individuals with
MS were selected. Complete data sets were obtained from 37
individuals with MS, three were eliminated from analyses due to
missing data.
The control group was selected from various community facilities
including clubs and social organisations. Complete data sets were
obtained from 38 controls, after three were eliminated with missing
data.
Controls were selected so that the distribution of age, gender and
socioeconomic status (SES) was approximately equal to the SLE and
MS groups (Table 2). None of the groups differed on the
demographic measures [age, F(2,105)=1.56, p=.21; SES, F(2,106)=1.21,
71
p=.30; gender, X2=1.64, df=2, p=.44; marital status 3, X2=2.12, df=2,
p=.351.
Table 2: Demographic characteristics of participants.
GENDER
SLE MS CONTROLS
males 6 7 11 females 28 30 27
AGE (years) mean 49.05 44.19 44.78 SD 16.24 8.19 12.14
MARITAL STATUS single 2 6 9 married/defacto/widowed 29 28 27 separated/divorced 3 3 2
DANIELS SCORE (OCCUPATIONAL SES; Daniels, 1983) mean 31.94 30.24 29.28 SD 7.48 4.97 8.82
All participants gave written informed consent to take part in the
study. A copy of the consent form appears in appendix one.
3.3.0 QUESTIONNAIRES
Only questionnaires derived from established psychological theories
and with robust psychometric properties were used in the study.
Copies of these questionnaires appear in appendix one. Since the
'The categories of single and separated/divorced were combined.
72
Sickness Impact Profile and the SCL-90—R have restricted availability,
they do not appear in the appendix.
DEMOGRAPHIC AND DISEASE HISTORY QUESTIONNAIRE
The demographic questionnaire asks respondents about their age, sex
and socioeconomic status as measured by the Daniels Score (Daniels,
1983). For individuals with SLE or MS, information about disease
duration, medication and disease status was also collected.
SOCIAL RESOURCES
The social resources measures used in the present study (short—hand •
variable names in brackets) were daily hassles [HASSLES], uplifts.
[UPLIFTS], social network [NETWORK] and social support
[SUPPORT].
DAILY HASSLES AND UPLIFTS SCALES [HASSLES & UPLIFTS]
Fifty—three items are rated for the amount of stress (hassles) and
pleasure (uplifts) they have provided in the past 14 days (Delongis,
Folkman & Lazarus, 1988). Although separate scales have been
devised to measure hassles and uplifts, it is recognised that a given
event may have both qualities. Recent research suggests hassles and
uplifts contribute differentially to disease outcomes, so there are
included as separate dependent variables in the present study
(Chamberlain & Zika, 1990).
73
NORBECK SOCIAL SUPPORT QUESTIONNAIRE [NETWORK]
The Norbeck Social Support Questionnaire was constructed to
measure network size, functional support and social losses. In the
present study, only the network size subscale is used since more
robust social support measures are available. To complete the
network measure, respondents list persons who are potential sources
of support and specify the nominated person's relationship (e.g.,
family, coworker or practitioner). The network subscale has a
test—retest reliability of .92 (Norbeck, Lindsay, & Carrieri, 1981).
INTERPERSONAL SUPPORT EVALUATION LIST [SUPPORT]
The Interpersonal Support Evaluation List (ISEL) comprises 40
statements concerning the availability of emotional, tangible,
belonging and appraisal social support. The tangible subscale
measures the availability of material aid; the appraisal subscale
assesses the availability of someone with whom to discuss problems;
the self—esteem subscale measures the availability of a positive
comparison when comparing one's self with others; and the
belonging subscale assesses the availability of people with whom one
can do things. The true/false format of the ISEL is counterbalanced,
with half the items inquiring about positive aspects of social support
and the other half about negative aspects. Scores on the four ISEL
subscales are summed to yield an estimate of total social support.
Test—retest reliabilities range between .63 and .70 for the individual
subscales and internal consistencies from .88 to .99. The ISEL has
74
documented discriminant and convergent validity (see Cohen,
Mermelstein, Kamarck & Hoberman, 1985).
PERSONAL RESOURCES
The personal resource measures adopted in the present study
(short-hand variable names in brackets) were self-efficacy
[EFFICACY], emotion-focused coping [EMOTION] and
problem-focused coping [PROBLEM].
SELF-EFFICACY [EFFICACY]
The 22-item Coppel (1980) scale has documented psychometric data
including internal validity (.91), test-retest reliability (.86),
convergent validity and factor structure. It measures behaviours
related to self-efficacy including behavioural maintenance and
outcome expectancies. It is a disposition measure and, therefore,
equally applicable to SLE, MS and healthy people. Self-efficacy levels
are reported as a single total score.
COPE [EMOTION & PROBLEM]
The COPE consists of 53 items that were derived from Lazarus and
Folkman's (1984) notion of emotional- and problem-focused coping
(Carver, et a., 1989). It consists of 13 subscales, 10 of which represent
three broad coping domains. These domains are active (or
problem-focused), supportive and maladaptive (emotion-focused)
coping and are not summed to yield a total COPE score. The
remaining three scales measure coping responses that are neither
75
adaptive nor maladaptive and are not included in the domain totals
or the present study. Individual COPE subscales have an internal
consistency ranging from .62 to .92, a two week test-retest reliability
of .61, as well as documented discriminant and convergent validity
(Caver et al., 1989).
Since the COPE assesses both the situational and dispositional aspects
of coping behaviour and is derived from the Folkman and Lazarus
model, it was chosen for the present study. To be consistent with the
Folkman and Lazarus model, only scores on the the emotion- and
problem-focused domains were used in the analysis. The subscales
that comprise problem-focused and emotion-focused coping domain
scores appear in Table 3.
DISEASE OUTCOMES
Outcome measures are the consequences of illness and include
(short-hand variable names in brackets) psychological distress
[DISTRESS], physical disability [PHYSICAL] and psychosocial
impairment [DISRUPTION].
PSYCHOLOGICAL DISTRESS [DISTRESS]
The revised 90 item Symptom Check-List (SCL-90-R) is a self-report
measure of current psychological distress, consisting of 90 items, each
rated on a five-point scale (Derogatis, 1983). The scale yields nine
primary symptom dimensions and three global scores of distress
(Table 4). The general symptom index (GSI) is considered the most
76
informative psychopathology measure and is adopted in the present
study (Brophy, Norvell & Kiluk, 1988). The SCL-90-R has a flexible
timeframe and in the present study psychological distress over the
past 14 days is assessed. The psychometric properties of the SCL-90-R
are robust and have been reviewed by Brophy and associates (Brophy
et al., 1988). A standardised SCL-90-R score of 63 is used to diagnose
clinical syndromes (Derogatis, 1977). The present study is concerned
with general (rather than clinical) distress levels and adopts the GSI
index rather than the cut-off criteria.
SICKNESS IMPACT PROFILE [PHYSICAL & DISRUPTION]
The SIP is a self-report measure of disability and psychosocial
disruption associated with medical conditions. Respondents are
asked to endorse only those items which describe their health over
the past 14 days (Bergner, 1977). Items are weighted according to the
severity of limitation on behaviour implied by each statement. The
items cover a range of domains including sleep and rest, eating,
work, home management, recreation and pastimes, ambulation,
mobility, emotional behaviour, body care and movement, social
interaction and communication. These subscales are summed to
yield a measure of psychosocial and physical disability, as well as an
overall sickness impact score.
The psychometric properties of the SIP are reviewed by Wilkin and
associates (Wilkin, Hallam & Doggett, 1992) and include high
internal consistency, test-retest reliability and inter-rater reliability.
77
Table 3: The problem—focused and emotion—focused COPE subscales. (After Carver et al., 1989)
PROBLEM-FOCUSED COPING
ACTIVE COPING Taking action, exerting efforts, to remove or circumvent the stressor.
PLANNING Thinking about how to confront the stressor, planning one's active coping efforts.
SUPPRESSION OF COMPETING ACTIVITIES Suppressing one's attention to other activities in order to concentrate on coping with the stressor.
POSITIVE REINTERPRETATION Making the best of a situation by viewing it in a more favourable light.
RESTRAINT Holding back one's coping efforts until they are effective.
EMOTION-FOCUSED COPING
ACCEPTANCE Accepting that the stressful event has occurred.
FOCUS ON & VENTING EMOTIONS Increased awareness of emotional stress and a tendency to vent emotional distress.
DENIAL Attempts to reject the reality of a stressful event.
MENTAL DISENGAGEMENT Psychological disengagement from the goal with which the stressor is interfering, through daydreaming, sleep, or self-distraction.
78
Table 4: The SCL-90—R symptom dimensions and global distress indices.
SOMATIZATION This dimension measures distress arising from bodily dysfunction.
OBSESSIVE—COMPULSIVE Measures thoughts, impulses and actions that are experienced as unremitting and irresistible.
INTERPERSONAL SENSITIVITY Focuses on feelings of personal inadequacy and inferiority.
DEPRESSION Measures symptoms indicative of depression including dysphoric mood, withdrawal, loss of interest in usual activities and decreased energy levels.
ANXIETY Assesses clinical signs of anxiety including nervousness, tension, panic attacks, feelings of terror and trembling.
HOSTILITY Measures thoughts, feelings or actions that characterise the state of anger.
PHOBIC ANXIETY This is a specific fear response to a person, place, object or situation which is characterised by irrational, avoidance or escape behaviour.
PARANOID IDEATION Measures paranoid behaviours including protective thought, hostility, suspiciousness, grandiosity, centrality and delusions.
PSYCHOTICISM This dimension measures behaviour indicative of schizophrenia and schizoid personality disorder. It assesses withdrawal, isolation, hallucinations and thought broad—casting.
GLOBAL INDICES OF DISTRESS 1. Global Severity Index (GSI) This score is considered the best single index of global distress, it combines information cri the number of symptoms and intensity of perceived distress.
2. Positive Symptom Distress Index (PSDI) The PSDI is a measure of distress intensity corrected for the number of symptoms reported.
3. Positive Symptom Total (PST) This assesses the number of symptoms reported independent of their severity.
79
The SIP also demonstrates high correlations with physician rated
disability. It has been used in over 40 studies of patients suffering
from various illnesses including chronic pain, arthritis, cancer,
angina, heart failure, fatigue and lung diseases (Wilkinet al., 1992).
Since the SIP assesses disability and psychosocial disruption resulting
from illness, it is easily administered to both SLE and MS sufferers, as
well as healthy controls. The present study uses physical disability
and psychosocial disruption scores as distinct disease outcome
measures. Examples of items comprising the physical SIP subscales
appear in Table 5.
3.4.0 PROCEDURE
Data were gathered by conducting personal interviews so as to
establish rapport and to insure completion of the questionnaires.
Since SLE and MS are uncommon medical conditions, it was
necessary to travel throughout Tasmania to interview the
volunteers. Interviews were conducted at sufferers' residences and at
a convenient time convient to the volunteer. For 95 percent of
individuals, two short interviews were arranged each lasting about
30-40 minutes. In the first interview rapport was established and
several questionnaires completed. An explanation of the remaining
questionnaires was then provided and individuals completed these
over a 10-14 day period. During the second interview, questionnaires
were scanned for their completeness and any questions volunteers
raised answered.
80
Table 5: Examples of items comprising the physical disability and psychosocial disruption subscales.
PHYSICAL DISABILITY BODY CARE & MOVEMENT I stand for only short periods of time. I do not maintain balance. I am in a restricted position all the time. I stay lying down most of the time.
MOBILITY I am getting around only within one building. I stay home most of the time. I stay away from home for only brief periods of time. I am staying in bed more.
PSYCHOSOCIAL DISRUPTION COMMUNICATION I am having trouble writing or typing I am understood with difficulty I do not speak clearly when I am under stress
EMOTIONAL BEHAVIOUR I act nervous or restless I talk about the future in a hopeless way I get sudden frights
One SLE and 10 MS sufferers reported visual problems or motor
difficulties. For these individuals several short visits were arranged
over a two week period where questions were read and answers
scribed.
81
Controls were screened for the presence of a chronic illness or
chronic symptomatology. Individuals in the healthy comparison
group received a financial reward for completing the questionnaires.
Questionnaires were scored according to their devised criteria and the
data analysed using SPSS (version 4) and Statview III.
(
82
Chapter Four
Results
83
The design consisted of three groups matched for age and socioeconomic
status. To control for Type I errors, group differences were first assessed
by performing a one—way multivariate analysis of variance (MANOVA)
on each group of dependent variables (social, personal and disease
outcome measures). To elucidate differences found to be significant by
MANOVA, one—way analyses of variance (ANOVA) and posthoc LSD
tests were preformed on each dependent variable to test differences
between pairs of means. The LSD tests were interpreted as significant
only if the preceding ANOVA was significant. Correlation matrices for
the separate groups were also determined. The significant correlations
are considered only briefly, as the purpose of the matrices is to explain
the possible processes underlying group differences.
Stepwise multiple regression was used to determine which social and
personal resource variables predicted disease outcomes and to establish
the strength of any relationships. These analyses were performed
separately for each group. An alpha level of .05 was adopted for all
statistical tests.
4.1.0 GROUP COMPARISONS
Table 6 contains means and standard deviations for the social, personal
and disease outcome measures. For the social measures the one-way
MANOVA was statistically significant [Wilks Lambda=.81, F
(8, 206)= 2.85, p=.0051]. Group differences were present for the uplifts
[F (2, 106)= 5.43, p=.00571 and social support [F (2, 106)= 4.54, p=.0127]
scales. Differences were attributable to SLE sufferers reporting fewer
84
uplifts than healthy controls or MS sufferers and the chronic illness
groups scoring lower on the social support scale (Table 7). No group
differences were evident on the hassles or network scales.
For personal resource measures, the one—way MANOVA was also
statistically significant [Wilks Lambda=.80, F(6, 208)= 3.94, p=.0009].
Group differences for the self—efficacy scale [F (2, 106)= 3.68, p=.0283] were
due to healthy controls scoring higher than either the SLE or MS groups
(Table 7). Differences on the emotion—focused coping scale
[F (2, 106)= 5.89, p=.0037] were due to controls using fewer of these
strategies than the SLE and MS groups (Table 7). There were no
significant group differences on the problem—focused coping scale.
Expected differences on the disease outcome measures were also present
[Wilks Lambda=.55, F (6, 208). 12.22, p=.0001]. All groups differed
statistically on the physical disability scale [F (2, 106). 24.81, p=.0001] with
the MS group reporting the highest and controls the lowest rates (Table
7). Significant differences on the psychosocial disruption measure
[F (2, 106). 17.69, p=.0001] arose from the SLE and MS groups scoring
higher than healthy controls (Table 7). Finally, differences on the
psychological distress measures [F (2, 106)= 21.13, p=.0001] arose from
controls reporting lower levels than the chronic illness groups (Table 7).
85
Table 6: Mean and standard deviation scores for social, personal and disease outcome measures.
SCALES
SOCIAL RESOURCES
SLE (n=34)
MS (n=37)
CONTROLS (n=38)
HASSLES mean 25.02 26.89 32.28 SD 19.93 17.64 24.40
UPLIFTS mean 35.52 43.13 53.89 SD 22.13 20.27 28.06
NETWORK mean 14.44 12.59 13.07 SD 6.77 8.31 5.94
SUPPORT mean 29.02 29.78 33.86 SD 8.58 8.62 4.36
PERSONAL RESOURCES EFFICACY
mean 62.17 62.05 68.21 SD 11.18 12.97 9.06
PROBLEM* mean 67.97 61.99 62.73 SD 13.63 14.98 16.71
EMOTION* mean 55.56 56.12 47.58 SD 10.63 9.73 14.81
DISEASE OUTCOME MEASURES DISTRESS
mean 60.29 62.75 48.02 SD 10.23 9.95 11.20
DISABILITY mean 5.51 16.11 0.39 SD 8.73 14.61 1.03
DISRUPTION mean 12.93 17.32 1.52 SD 13.77 15.16 3.10
PROBLEM*= Problem-focused coping, EMOTION*= emotion-focused coping
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Table 7: Univariate comparisons and post hoc tests for social, personal and disease outcome measures
for the control (C), SLE and MS groups.
SCALES
SOCIAL RESOURCES
df p LSD*
HASSLES 1.19 2,106 .3082 C>MS>SLE
UPLIFTS 5.43 2,106 .0057 C>MS>SLE
NETWORK .64 2,106 .5281 SLE >C>MS
SUPPORT 4.55 2,106 .0127 C>MS>SLE
PERSONAL RESOURCES EFFICACY 3.69 2,106 .0283 C>SLE>MS
PROBLEM* 1.62 2,106 .2043 SLE>C>MS
EMOTION* 5.89 2,106 .0037 MS>SLE>C
DISEASE OUTCOME MEASURES DISTRESS
21.13 2,106 .0001 MS>SLE>C
DISABILITY 24.81 2,106 .0001 MS>SLE>C
DISRUPTION 17.69 2,106 .0001 MS>SLE>C
*Groups with a common underline do not have significantly different means
PROBLEM*= Problem-focused coping, EMOTION*= emotion-focused coping
4.2.0 RELATIONSHIPS BETWEEN THE VARIABLES
The correlation matrices for the separate groups are presented in Table 8,
with statistically significant coefficients being indicated by bold type.
More variables were significantly correlated for the control group and
fewer for the SLE sufferers. The dissimilar correlation patterns are
87
considered further in the discussion as explanations for the group
differences observed above.
4.3.0 PREDICTING DISEASE OUTCOMES
Stepwise multiple regression was used to determine which social and
personal resource variables predicted disease outcomes and to establish
the strength of their relationships. An inspection of the correlations
between variables (Table 8) suggests they interact differentially to
influence disease outcomes for the different groups. Consequently
stepwise regressions were performed separately for each group. An
F—to—enter value of 4.17 was derived from the degrees—of—freedom for
the smallest group [SLE sufferers df=(1,32)].
DISTRESS
For the SLE group, social and personal resources were not correlated
with psychological distress scores. In the stepwise analysis, however,
hassles and uplifts predicted psychological distress scores (Table 9). At
step one hassle scores were entered into the equation R 2 = .18, [F (1, 32)
= 7.12, p<.051. Uplifts were entered at step two 1R 2 = .30, [F (2,31) = 6.51,
p<.01]. No additional variables were entered into the equation. The
standardised regression coefficients suggest decreasing uplifts and
increasing hassles are associated with elevated psychological distress.
For the MS group, none of the observed social and personal variables
were significantly correlated with the measure of psychological distress
(Table 9).
88
Table 8: Correlation matrices for SLE (n=34), MS (n=37) and control (n=38) groups*.
SLE A B C D E F G H I HASSLES A UPLIFTS B .07 NETWORK C -.11 .11 SUPPORT D -.51 .06 .23
EFFICACY E -.11 .23 -.12 .30 PROBLEM* F -.01 .27 -.00 .22 . 3 6 EMOTION* G .27 .00 -.25 -.14 .08 .55
DISTRESS H . 4 3 -.31 -.13 -.35 -.34 -.22 .22 DISABILITY I .27 -.08 .11 -.26 -.13 .16 .04 .12 DISRUPTION I . 6 9 -.07 .01 -.46 -.26 -.07 .21 .54 . 6 2
MS A B C D E F G H I HASSLES A UPLIFTS B . 3 6 NETWORK C -.08 .23 SUPPORT D -.17 . 3 6 .26
EFFICACY E -.09 .21 .17 . 4 8 PROBLEM* F -.13 . 5 1 .26 . 4 4 . 6 1 EMOTION* G .12 .28 .26 .25 .10 .49
DISTRESS H .23 .22 .10 -.28 -.29 -.02 -.03 DISABILITY I -.06 -.17 -.15 -.56 -.13 -.13 -.26 .33 DISRUPTION! .19 -.19 .17 -.54 -.53 -.30 .06 .64 . 4 6
CONTROLS A B C D E F G H I HASSLES A UPLIFTS B . 3 7 NETWORK C -.19 .30 SUPPORT .D -.30 .15 . 4 2
EFFICACY E -.16 .00 .10 . 4 1 PROBLEM* F .28 . 7 5 .23 .02 -.01 EMOTION* G . 5 4 . 6 1 -.07 -.34 -.36 .69
DISTRESS H .31 .10 -.48 -.54 -.41 .21 .60 DISABILITY I .05 -.14 -.24 -.08 -.08 .02 -.12 -.04 DISRUPTION J . 4 6 .10 -.10 -.21 -.15 .36 . 3 3 .43 .23
* Statistically significant correlations (p<.05) are in bold type PROBLEM*= Problem-focused coping, EMOTION*= emotion-focused coping resource measures
89
Table 9: Summary of the stepwise regression for variables predicting psychological distress.
Variable SE B
SLE Hassles .23 .08 .45 RZ=.30 Uplifts -.15 .07 -.34
MS No significant predictors
CONTROLS Emotion* .43 .09 .57 R-Z=.56 Network -.83 .21 -.44
Emotion*=emotion-focused coping
For control controls, emotion-focused coping, social support and
network size were correlated with psychological distress (Table 8). In the
stepwise analysis, emotion-focused coping was first entered into the
equation R2 = .36, [F (1, 36) = 20.56, p<.011 (Table 9). At step two,
network size was entered 1 2 = .56, [F (2, 35) = 21.98, p<.01]. After step
two, the remaining variables did not have an F-value greater than 4.17
and were not entered into the equation. The standardised regression
coefficients indicated that a small social 'network and more
emotion-focused coping was associated with higher psychological
distress scores for control controls.
PHYSICAL DISABILITY
For the SLE group, social and personal resource measures were not
correlated and did not predict physical disability levels. For the MS
90
group, however, social support was significantly correlated with and
predicted physical disability levels E.2 = .32, [F (1, 35) = 16.18, p<.01].
From the standardised regression coefficient (Table 10) more physical
disability was associated with less social support. For control group,
social and personal resource measures were not correlated and did not
predict physical disability levels.
Table 10: Summary of the stepwise regression for variables predicting physical disability levels.
Variable
SE B
SLE No significant predictors
MS
Social support -.95 .24 -.56 R-Z=.32
CONTROLS No significant predictors
PSYCHOSOCIAL DISRUPTION
For the SLE group, disruption was correlated with hassles and social
support. However, hassle levels were the only significant predictor of
psychosocial disruption for SLE sufferers a2 = .48, [F (1, 32) = 28.99,
p<.01] (Table 11). Higher hassle levels were associated with more
psychosocial disruption.
Social support and self-efficacy were significantly correlated with
disability levels for MS volunteers. These, in addition to network size,
predicted psychosocial disruption levels (Table 11). Social support was
entered at step one a2 = .29, [F (1, 35) = 14.06, p<.01], network size at step
91
two 1R2 = .39, [F (2, 34) = 10.81, p<.01] and self-efficacy levels at step three
R2 = .50, [F (3, 33) = 10.84, p<.01]. Higher psychosocial disruption levels
were associated with less social support and self—efficacy, as well as a
larger network size.
Table 11: Summary of the stepwise regression for variables predicting psychosocial disruption.
Variable SE B
SLE Hassles .48 .08 .68 RZ=.48
MS Support -.79 .25 -.45 RZ=.50 Network .64 .23 .35
Efficacy -.44 .16 -.37
CONTROLS Hassles .06 .02 .46 RZ=.21
For healthy controls, emotion— and problem—focused coping were
correlated with disruption scores for healthy controls. Nevertheless,
hassle levels were the only significant predictor of psychosocial
disruption for the control group R2 = .21, [F (1,36) = 9.82, p<.01]. Where
a moderate increase in hassles were associated with more psychosocial
disruption. This finding is, however, unreliable given the large
proportion of participants scoring zero disruption.
92
Chapter Five
Discussion
93
5.1.0 OVERVIEW
The discussion parallels the results section, commenting first on the
group differences for social, personal and disease outcome measures. For
several measures, the limited research with SLE sufferers makes the
findings difficult to interpret theoretically. By comparing Correlation
matrices (Table 8), however, some provisional hypotheses about the
processes underlying group differences can be generated. The second
section discusses the significance of social and personal variables in
predicting disease outcome measures.
5.2.0 GROUP COMPARISONS
SOCIAL RESOURCES
The MANOVA for social resource measures was statistically significant.
Group differences were present for the uplifts and social support scales,
but not of the hassle or network measures.
HASSLES
Although significant group differences were not evident on the hassles
(stress) measure, controls reported marginally higher rates than the illness
groups. This finding is contrary to the prediction that stress levels would
be substantially elevated in the illness groups and may be reconciled by
examining the methodology of published research.
Published research implies that high stress precedes disease exacerbations,
but does not consider whether levels differ from other chronic illnesses
94
or 'healthy' controls (e.g., Laing et al., 1984; Rimon & Kronqvist, 1988).
These studies also use hospitalised samples and may, therefore, be biased
towards individuals with few coping skills or a more serious illness.
Furthermore, they neglect to consider possible confounding between
symptomatology, recent changes in the availability of social support and
stress (see Thoits, 1985 for a review).
There also may be behavioural explanations for the observed differences
in reported stress levels. For example, SLE sufferers may implicitly or
explicitly avoid stress as they are more susceptible to its deleterious effects.
Alternatively, being chronically ill may limit the range of activities in
which individual can participate and hence the potential for stress.
Taking account of activity levels would thus be more appropriate for
assessing the effects of stress.
The interaction of hassles with the other variables provides another
explanation of the possible processes underlying group differences. For
the SLE group, high stress and low social support lead to psychological
distress and psychosocial disruption. This finding is consistent with the
buffering hypothesis of social support and is widely supported by research
(see Cohen & Wills, 1985 for a review). High stress levels were associated
with more positive events for MS sufferers, but not with disease outcome
measures. This suggests high activity levels are both pleasurable and
stressful for MS sufferers but are less important to disease outcome. For
95
controls, high stress [and uplifts] in the presence of emotion—focused
coping leads to psychosocial disruption.
Whereas studies suggest SLE sufferers experience elevated stress levels,
this finding may result from methodological limitations such as a lack of
comparisons groups, using seriously ill hospitalised sufferers and
confounded stress assessments. The low stress levels also may result from
behavioural factors such as leaving the work force or avoiding potentially
stressful activities. Correlational data suggest stress in the absence of
sufficient social support may lead to psychological distress in SLE sufferers.
UPLIFTS
Whereas SLE research uses daily hassle methodology, the
contradistinction that uplifts (or positive events) are important predictors
of disease outcome is not widely investigated. Using the latter measure,
significant differences in the number of uplifts were evident with controls
differing from the chronic illness groups.
This finding is consistent with the notion that chronic illness limits
activity and hence access to pleasurable events. Cognitive styles that
disregard the positive aspects of events or high psychological distress
levels also may influence reporting of pleasurable events, with distressed
individuals reporting fewer pleasurable events (Macgillivray & Baron,
1994).
96
The interaction of uplifts With other variables may also suggest reasons for
group differences on the scale. Uplifts were not correlated with any social,
personal or disease outcome measure for the SLE group. Thus, uplifts are
less important to the well-being of SLE sufferers. For the MS group,
uplifts are associated with more social support, problem-focused coping
and stress. They were, however, unrelated to the disease outcome
measures. Thus, for individuals with MS, activity levels may depend on
the presence of social support which in turn promotes problem-focused
coping. Uplifts were associated with more stress, problem- and
emotion-focused coping for the control group. For controls, high activity
levels promote both more positive and negative coping strategies.
SOCIAL NETWORKS AND SOCIAL SUPPORT
Although not statistically significant, SLE sufferers reported more social
network members than either control or MS subjects. This finding is
interesting as it suggests that there has been no decrease in network size in
the SLE group over the course of the disease. When compared with the
illness groups however, control subjects reported significantly more social
support. Thus, despite embeddedness in a social network, chronic illness
sufferers may received less social support than healthy people. The
correlation matrices may provide insight into how and why social
relationship vary between the groups.
For healthy controls, social support is influenced differentially by social
and personal resource variables. Social network size and social support
97
are highly correlated, suggesting embeddedness is associated with
potentially more social support. High social support also is associated
with greater self—efficacy and using less emotion—focused coping. Low
social support and a small network are related to increased psychological
distress, but not to the other disease outcome measures. Causal
associations aside, the intercorrelations between variables suggest that low
self-efficacy and emotion—focused coping in the presence of low social
support are associated with less psychological distress in healthy people.
For the SLE group, social support is associated with different social and
personal resource variables. Lower social support was associated with
more stress and psychosocial disruption. That is, there was evidence for
the buffering model of social support.
For MS sufferers, high social support was significantly associated with
greater self—efficacy, problem—focused coping and more uplifts. The
aforementioned correlations suggest that positive events are associated
with greater self—efficacy which improves problem—focused coping and
enhances social support levels. This hypothesis has some support from
the notion that social support promotes coping assistance which in turn
minimises negative disease outcomes (Thoits, 1986).
Another important implication from these post hoc analyses is that social
support is differentially related to disease outcome measures. For control
subjects, low social support was associated with more psychological
98
distress, but not the other indices of health status. This finding is
unsurprising given that controls were selected for their absence of ill
health. For SLE sufferers, high social support was associated with less
psychosocial disruption, but not with psychological distress or disability.
Thus, high social support may have a buffering role against psychosocial
disruption. Equally low levels of social support may be a consequence of
psychosocial disruption. For the MS group, low social support was
associated with greater physical disability and psychosocial disruption and
unrelated to psychological distress scores. It is possible that high disability
mitigates social support levels which in turn lead to increases in
psychosocial disruption (Brown et al., 1989).
Although it was theoretically possible to investigate the buffering
hypothesis for social support in the present study, this is not
recommended when data is cross-sectional (Felner et al., 1983; Thoits,
1985; Cohen & Wills, 1985; Gottieb, 1988). Cross-sectionally, high stress
levels have been a demonstrated consequence of low social support and
low stress levels are correlated with high social support (Felner et al., 1983;
Thoits, 1985; Cohen & Wills, 1985; Gottieb, 1988). Thus, preexisting stress
levels may be an outcome of existing social support. Furthermore, high
stress levels may arise from a loss of social support, again confounding
outcomes. The aforementioned difficulties make longitudinal data that
controls for time-1 levels of stress and social support the minimal
requirement for testing the buffering hypothesis (Felner et al., 1983;
Thoits, 1985; Colien et al., 1985; Cohen & Wills, 1985; Gottieb, 1988; Brown
99
et al., 1989; Fitzpatrick et al., 1991).
PERSONAL RESOURCES
The MANOVA for personal resource measures was statistically significant.
Group differences were present for the self—efficacy and emotion—focused
coping scale, but not of the problem—focused coping measure.
SELF—EFFICACY
The prediction that self—efficacy levels would be significantly higher for
controls than for either illness group was supported. The antecedents of
lowered levels are not evident from this study, but it is likely that the
unpredictable relapsing and remitting course of SLE may lower
self—efficacy perceptions as individuals believe they lack the skills to
alleviate symptomatology.
The group differences may again be clarified by considering the association
of efficacy with other variables. For both chronic illness groups,
problem—focused coping was significant related to self—efficacy. This
finding also has been reported with RA sufferers (Schiaffino et al., 1991).
For SLE sufferers, self—efficacy was not significantly related to any other
social, personal or outcome variables. For individuals with MS, high
self—efficacy was related to low disability which is consistent with findings
from other studies (O'Leary et al., 1988; Schiaffino et al., 1991). High
self—efficacy also was significantly related to higher social support which is
again consistent with the findings from other studies (O'Leary et al., 1988).
100
Thus, for SLE sufferers high self-efficacy may promote problem-focused
coping or vice versa, and for MS sufferers this relationship is further
mediated by high social support and disability levels.
For controls high self-efficacy was correlated with high social support. It
also was correlated with using fewer emotion-focused coping strategies,
but not with problem-focused coping. Thus, self-efficacy may promote
social support and limit unproductive emotion-focused coping.
PROBLEM- AND EMOTION-FOCUSED COPING
No significant group differences were present on the problem-focused
coping measure. Significant group differences on the emotion-focused
coping measure were evident. The chronic illness group used more
emotion-focused strategies than control subjects. Thus, chronically ill
individuals use problem-focused strategies as often as healthy controls.
They also use more emotion-focused strategies that are less advantageous
to overall well-being. This finding is not widely reported, as most
researchers classify individuals as either emotion- or problem-focused
copers to compare outcome measures (e.g., Brown et al., 1989; Revenson &
Felton, 1989; Newman et al., 1990). This typology is not justified in the
present study as emotion- and problem-focused coping were highly
correlated in all the groups (Table 8).
Group differences in coping strategies also may be clarified by considering
their association with other variables. For the chronic illness groups,
101
individuals using problem—focused coping strategies reported higher
self—efficacy scores. No evidence was found for the previously reported
finding that emotion—focused coping would be significantly associated
with either low self—efficacy [or high disability] scores (Revenson &
Felton, 1989). No other significant associations between coping and the
other variables were evident for SLE sufferers. For the MS group, high
scores on the problem—focused coping scale were associated with more
positive events and social support. Furthermore, individuals with high
scores on the emotion—focused coping scale reported less psychosocial
disruption. Finally, in the chronic illness groups no support was found
for problem—focused coping being associated with lower disability levels
(Newman et al., 1990), emotion—focused coping being associated with
more psychological distress (Brown et al., 1989) or problem—focused
coping being associated with less psychological distress (Brown et al.,
1989).
For controls, coping was complexly related to the other variables. Higher
problem—focused coping scores were associated with more uplifts and
psychosocial disruption. Higher emotion—focused coping scores were
associated with more hassles, uplifts, psychological distress and
psychosocial disruption. Emotion—focused coping also was associated
with less social support and lower self—efficacy scores. Thus, it appears
that when coping is important, both emotion— and problem—focused
coping strategies are employed. Individuals with higher emotion—focused
scores, however, experience lower social support and lower self—efficacy
102
levels. It is implicit from the correlation matrix for controls that
emotion—focused coping may be adaptive at low levels, but detrimental to
personal or social resources when used extensively. The COPE scale may
also have multicollinearity problems, with emotion—focused items
overlapping with measures of social support, psychological distress and
psychosocial disruption.
DISEASE OUTCOME MEASURES
The MANOVA for disease outcome measures was statistically significant.
Group differences were present for the psychological distress, disability
and psychosocial disruption measures.
PSYCHOLOGICAL DISTRESS
The prediction that chronic illness would be associated with more
psychological distress was supported, with distress levels being comparable
between SLE and MS sufferers, who both differed significantly from
controls.
For the SLE group, psychological distress was associated with more hassles
and psychosocial disruption. These findings have been widely reported
(e.g. Otto & Mackay, 1967; Laing et al., 1984; Rimon & Kronqvist, 1988;
Wekking et al., 1991) in SLE sufferers. Curiously, other social and personal
resources variables were not associated with psychological distress scores
suggesting specific etiological factors in SLE sufferers. For the MS group,
higher psychological distress was related to more psychosocial disruption.
103
No other significant correlations were evident for MS sufferers. For
controls, high psychological distress was associated with a smaller social
network and less social support. These findings have been widely
reported in studies with healthy people (see Cohen & Wills, 1985 for a
review). Psychological distress also was associated with using more
emotion—focused coping and greater psychosocial disruption.
DISABILITY AND PSYCHOSOCIAL DISRUPTION
The groups were significantly different on the disability measure with MS
sufferers scoring higher than SLE, who in turn differed from controls.
This finding is unremarkable as controls subjects were selected for the
absence of illness. The higher score of MS sufferers was also expected, as
this group experiences more mobility problems than SLE sufferers.
Psychosocial disruption scores for the chronic illness groups also differed
significantly from controls. With scores of SLE and MS sufferers being
comparable due to symptomatology causing disruption independently of
its etiology. The lower scores for control subjects are unremarkable as this
group were free from ill health.
The Disease Exacerbation Model predicted a deterioration in all social and
personal resources as well as in disease outcomes. While significant
decrements were observed on all disease outcome measures when
comparing the chronic illness and control groups, there were some social
and personal resources not apparently influenced by the course of disease.
104
In particular, there was no significant difference between the chronic
illness and control groups on measures of hassles, network size or
problem—focused coping. These findings provide a significant
qualification in refining the scope of the Disease Exacerbation Model for
chronic illness.
5.3.0 PREDICTORS OF DISEASE OUTCOME
While group differences may be partially explained by the differential
interaction of variables, their importance in disease outcome was
established through stepwise multiple regression analyses. The discussion
again parallels the results section format.
PSYCHOLOGICAL DISTRESS
For the SLE group, hassles in the absence of uplifts predicted psychological
distress and accounted for 30 percent of the variance. Uplifts appear to
have a buffering or compensatory effect in that they were not significantly
associated with psychological distress in the correlation matrix (Table 8). It
is consistent with studies using 'healthy people' and the theoretical
underpinnings of hassle and uplift research proposed by Delongis and
associates (1988). That is, high stress in the absence of counterbalancing
uplifts (positive events) leads to psychological states such as anxiety and
depression as well as physical symptomatology (Delongis et al., 1988).
There were no predictors for psychological distress in the stepwise model
for MS sufferers. This finding is consistent with correlational data. That
105
is, psychological distress was not significantly correlated with either social
or personal resource variables. Thus psychological distress in MS sufferers
is influenced by variables not included in the current model and has a
different etiology than for the SLE group.
For the control group, emotion—focused coping and a small social network
predicted psychological distress. These variables accounted for 56 percent
of the observed variance for psychological distress scores. This etiology is
different to the hassles and uplifts model observed in SLE sufferers, and
implies a main—effect for social networks in the presence of poor coping
(Cohen & Wills, 1985).
PHYSICAL DISABILITY
For the SLE and control groups, neither social nor personal resources
predicted disability scores. Since controls were selected for an absence of
illness and hence disability, the null relationship is not unexpected. The
lack of a significant relationship for SLE sufferers suggests that disability
levels are not mediated by social and personal resources for SLE sufferers.
For individuals with MS, however, insufficient social support predicted
higher disability scores and accounted for 32 percent of the variance. This
suggests that social support is important in assisting individuals to
overcome mobility and related problems (Wineman, 1990).
PSYCHOSOCIAL DISRUPTION
-For controls and SLE sufferers, high hassles were associated with more
106
psychosocial disruption. For the SLE group, 48 percent of psychosocial
disruption was attribute to hassles and is consistent with research findings
(e.g. Otto & Mackay, 1967; Laing et al., 1984). For the MS group, 50 percent
of psychosocial disruption was attributable to low social support in the
presence of a large social network and poor self-efficacy.
5.4.0 SUMMARY AND CONCLUSIONS
This study examined the social, personal and disease outcome differences
between SLE, MS and healthy control subjects. This comparative design
provided partial support for the Disease Exacerbation Model of chronic
illness. It demonstrated that individuals with SLE experienced similar
problems to MS sufferers (with the exception that MS sufferers reported
significantly more disability) and that both illness groups differed from
healthy controls.
Both chronic illness groups reported less social support, more
emotion-focused coping and lower self-efficacy. In addition, the chronic
illness groups reported more psychological distress, disability and
psychosocial disruption. No significant differences were, however, found
between the chronic illness groups and healthy controls on the hassles,
network size, or problem-focused coping measures. Some social and
personal resources of ill people, therefore, remained intact despite
suffering from a chronic disease.
107
The correlation matrices demonstrated that social, personal and disease
outcome measures interact differentially to influence group differences.
These interactions are, however, best investigated longitudinally
controlling for time-1 levels of the variables. For example, the buffering
hypothesis could not be adequately investigated with cross-sectional data
as high stress has been demonstrated to be a function of low social support
levels (Thoits, 1985; Cohen & Wills, 1985).
For the SLE group, hassles appear to be the most important moderator of
disease outcome, but may be buffered by uplifts. Social support also was
significantly related to psychosocial disruption and may be a mitigating
factor. For MS sufferers, social support, networks and self—efficacy are the
important social and personal resource variables mediating disease
outcomes. While useful for comparison purposes, the regression
findings are less unreliable for controls, as these individuals were free
from chronic illness.
There are several methodological problems in this present study that limit
the generalisation of findings. Individual matching was not possible in
the present study because of limitations of available participants in the
chronic illness groups. Furthermore, other social and personal resources
not included in the present study may also be important mediators of
disease outcomes. These include social resources such as negative social
support transactions, as well as the personal resources such as cognitive
styles and control. Finally, some of the hypotheses of interest in studying
108
the course of chronic illness are not adequately tested in a cross—sectional
designs. For example, the buffering hypothesis for social support requires
longitudinal data for adequate assessment. Despite these limitations, the
present study has contributed to the identification of social and personal
resources impacted upon by the process of two chronic diseases. It also has
identified which social and personal resources potentially act as mediators
in the disease process and has implications for intervention studies that
may influence the course of chronic illness.
109
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119
APPENDIX ONE QUESTIONNAIRES
Consent Form 120
Medical and Demographic Questionnaires
Revised Diagnostic Criteria for Systemic Lupus Erythematosus 121-122
Demographic Information 123
Disease History Questionnaire 124-125
Social Resource Measures
Hassles and Uplifts Scale 126-129
Social Network (NSSQ) Measure 130
Social Support (ISEL) Questionnaire 131-133
Personal Resource Measures
Self-Efficacy Scale 134-135
COPE 136-138
120
Social and Personal Resources as Mediators of Disease Outcome in Chronic Illness and Healthy People
CONSENT FORM
You are probably aware that having systemic lupus erythematosus (SLE)/multiple sclerosis (MS) may effect the quality of your life. Disruptions to life style could arise from disability, pain, restricted social contacts, your fatigue or medication. These stresses may make it more difficult to cope, lead to anxiety or depression and prolong exacerbations.
Research is currently underway investigating how SLE /MS effects the quality of your life. The study is open to people with SLE/MS throughout Tasmania, irrespective of the severity of your condition or where you live. The study is currently underway and involves two short interviews and some questionnaires to complete in your own time. A research assistant will visit you at home and help you to complete the questionnaires. If this is inconvenient other arrangements can be made. All information you provide will be kept confidential and only group data will be reported in scientific publications. You may withdraw from the study at any time, if you wish to do so.
If you would like more information you can contact Helen Hornsby Ph. (002) 202889 during office hours or the SLE/MS Society.
I have read and understand the consent form
Name
Address
Signature Date
Witness
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REVISED DIAGNOSTIC CRITERIA FOR SYSTEMIC LUPUS ERYTHEMATOSUS
:ed below is the diagnostic criteria for systemic lupus erythematosus. Please Eorse the symptomatology your patient suffers, by ticking the appropriate box [ 1. our patient is not a systemic lupus erythematosus sufferer, but fits some of the )w criteria, endorse the appropriate symptomatology. Over the page is a place for [ to specify your patient's diagnosis.
Criterion Definition
[ ] Malar Rash Fixed erythema, flat or raised, over the malar eminences, tending to spare the nasolabial folds.
[ ] Discoid Lupus Erythematosus raised patches with adherent keratotic scaling and follicular plugging; atrophic scaring may occur in older lesions.
Photosensitivity Skin rash as a result of unusual reaction to • sunlight, by patient history or physician observation.
[ ] Oral ulcers Oral or nasopharyngeal ulceration, usually painless, observed by physician.
[ ] Arthritis Nonerosive arthritis involving two or more peripheral joints, characterised by tenderness, swelling, or effusion.
Serositis a.Pleuritis- convincing history of pleuritic pain or rub heard by a physician or evidence of pleural effusion OR
b.Pericarditis- documented by ECG or rub or evidence or pericardial effusion.
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Renal a. Persistent proteinuria greater than 0.5g/day or Disorder
greater than 3+ if quantitation not performed OR
b. Cellular casts- may be red cell, hemoglobin, granular, tubular, or mixed.
Neurologic a. Seizures- in the absence of offending drugs or Disorder
known metabolic derangements; e.g., uremia, ketoacidosis, or electrolyte imbalance OR
b. Psychosis- in the absence of offending drugs or known metabolic derangements; eg., uremia, ketoacidosis, or electrolyte imbalance.
Hematologic a. Hemolytic anemia- with reticulocytosis Disorder OR
b.Leukopenia- less than 4000/mm3 total on two or more occasions OR
c.Lymphopenia- less than 1500/mm3 on two or more occasions OR
d.Thrombocytopenia- less than 100,000/mm3 in the absence of offending drugs.
Immunologic a. Positive LE cell preparation Disorder OR
b.Anti-DNA: antibody to native DNA in abnormal titer OR
c.Anti-Sm: presence of antibody to S m nuclear antigen OR
d.False-positive serologic test for syphilis known to be positive for at least 6 months and confirmed by Treponema pallidum immobilization or fluorescent treponemal antibody absorption test.
Antinuclear An abnormal titer of antinuclear antibody by Antibody immunofluorescence or an equivalent assay at
any point in time and in the absence of drugs known to be associated with "drug-induced lupus" syndrome.
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DEMOGRAPHIC INFORMATION
Gender: Female [ ] Male [ ] Age
Marital Status: single [ I
married [ I
separated [ I
divorced [ ]
widowed [ I
Do you live (tick as many as apply):
on your own [ I
with your spouse partner [ ]
with friends [ I
with brothers and/or sisters [ ]
with parents [ i
with your children [ I
other, specify
Occupation
If a dependent, breadwinner's occupation
If a pensioner or unemployed, previous occupation
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How old were you when diagnosed?
How long before diagnosis did you suffer from lupus/MS?
List any medication(s) prescribed to relieve your symptoms over the past 6 months. Include the dosage level, frequency of ingestion, and how long you have been taking each medication.
a. medication b. medication
dosage dosage
frequency frequency
duration_ duration
c. medication._ d. medication
dosage dosage
frequency frequency
duration_ duration
To what extent do the following medication side effects interfere with your daily functioning (e.g. ability to do housework, work or socialise).
a. increased appetite or weight gain
no disruption severe disruption
b. depression
no disruption severe disruption
c. stomach irritations
no disruption severe disruption
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d. fluid retention or moon face
no disruption severe disruption
e. dizziness
no disruption severe disruption
f. slow healing injuries
no disruption severe disruption
g. being easily bruised
no disruption severe disruption
Lupus/MS is characterised by periods of flare and remission. A flare occurs when your symptoms increase in intensity, possibly causing you considerable discomfort and distress. Remission occurs when there is an interval or break in the intensity of your symptoms, your discomfort is usually reduced.
What is your current illness condition?
flare
remission
early stage of a flare
late stage of a flare
never experienced a flare
"under control" (i.e., medication is preventing a flare)
not sure
[
[
[ 1
[ 1
[ 1
[
[ 1
About how long have you experienced your current (as above) illness condition?
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INSTRUCTIONS
HASSLES are irritants things that annoy or bother you; they can make you upset or angry. UPLIFTS are events that make you feel good; they can make you joyful, glad, or satisfied. Some hassles and uplifts occur on a fairly regular basis and others are relatively rare. Some have only a slight effect, others have a strong effect.
This questionnaire lists things that can be hassles and uplifts in day-to-day life. You will find that during the course of a day some of these things will have been hassles for you and some will have been only an uplift. Others will have been both a hassle AND an uplift.
DIRECTIONS: Please think about how much of a hassle and how much of an uplift each item was for you today. Please indicate on the left-hand side of the page (under "HASSLES") how much of a hassle the item was by circling the appropriate number. Then indicate on the right-hand side of the page (under "UPLIFTS") how much of an uplift it was for you by circling the appropriate number.
Remember, circle one number of the left-hand side of the page and one number on the right-hand side of the page for each item.
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HASSLES AND UPLIFT SCALE
How much of a hassle was How much of an uplift was this item for you today? this item for you today?
HASSLES UPLIFTS 0 = None or not applicable None or not applicable =0 1 = Somewhat Somewhat = 1 2= Quite a bit Quite a bit = 2 3 = A great deal A great deal = 3
0 1 2 3 1. Your child(ren) 0 1 2 3
0 1 2 3 2. Your parents or parents-in-law 0 1 2 3
0 1 2 3 3. Other relative(s) 0 1 2 3
0 1 2 3 4. Your spouse 0 1 2 3
0 1 2 3 5. Time spent with your family 0 1 2 3
0 1 2 3 6. Health or well-being of a family member
0 1 2 3
0 1 2 3 7. Sex 0 1 2 3
0 1 2 3 8. Intimacy 0 1 2 3
0 1 2 3 9. Family related obligations 0 1 2 3
0 1 2 3 10. Your friend(s) 0 1 2 3
2 3 11. Fellow workers 0 1 2 3
0 1 2 3 12. Clients, customers, patients, etc. 0 1 2 3
0 1 2 3 13. Your supervisor or employer 0 1 2 3
0 1 2 3 14. The nature of your work 0 1 2 3
0 1 2 3 15. Your work load 0 1 2 3
0 1 2 3 16. Your job security 0 1 2 3
0 1 2 3 17. Meeting deadlines or goals on the job 0 1 2 3
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HASSLES UPLIFTS
HASSLES
UPLIFTS
0 = None or not applicable None or not applicable =0 1= Somewhat Somewhat =1 2 = Quite a bit Quite a bit = 2
3 = A great deal A great deal =3
0 1 2 3 18. Enough money for necessities (e.g., food, clothing, housing, health care, taxes, insurance)
0 12 3
0 1 2 3 19. Enough money for education
0 1 2 3 20. Enough money for emergencies
0 1 2 3 21. Enough money for extras (e.g., entertainment, recreation, vacations)
1 2 3 22. Financial care for someone who doesn't live with you
0 1 2 3 23. Investments
0 1 2 3 24. Your smoking
0 1 2 3 25. Your drinking
0 1 2 3 26. Mood-altering drugs
0 1 2 3 27. Your physical appearance
0 1 2 3 28. Contraception
0 1 2 3 29. Exercise(s)
0 1 2 3 30. Your medical care
0 1 2 3 31. Your health
0 1 2 3 32. Your physical abilities
0 1 2 3 33. The weather
0 1 2 3 34. News events
0 1 2 3 35. Your environment (e.g., quality of air, noise level, greenery)
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HASSLES UPLIFTS
0= None or not applicable None or not applicable =0 1 = Somewhat Somewhat =1 2 = Quite a bit Quite a bit = 2 3 = A great deal A great deal =3
0 1 2 3 36. Political or social issues 0 1 2 3
0 1 2 3 37. Your neighbourhood (e.g., neighbours, setting)
0 1 2 3
0 1 2 3 38. Conserving (gas, electricity, water petrol etc.)
0 1 2 3
0 1 2 3 39. Pets 0 1 2 3
0 1 2 3 40. Cooking 0 1 2 3
0 1 2 3 41. House work 0 1 2 3
0 1 2 3 42. Home repairs 0 1 2 3
0 1 2 3 43. Yardwork 0 1 2 3
0 1 2 3 44. Car maintenance 0 1 2 3
0 1 2 3 45. Taking care of paperwork (e.g., paying bills, filling of forms)
0 1 2 3
0 1 2 3 46. Home entertainment (e.g., TV, music, reading)
0 1 2 3
0 1 2 3 47. Amount of free time 0 1 2 3
0 1 2 3 48. Recreation and entertainment outside home (e.g., movies, sports, eating out, walking)
0 1 2 3
0 1 2 3 49. Eating (at home) 0 1 2 3
0 1 2 3 50. Church or community organisations 0 1 2 3
0 1 2 3 51. Legal matters 0 1 2 3
0 1 2 3 52. Being organised 0 1 2 3
0 1 2 3 53. Social commitments 0 1 2 3
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NSSQ
List each significant person in your life. Consider all the persons who have been important to you in the past 6 months. When listing individuals use only their first name or initials. Additionally, specify your relationship (e.g., spouse, family or relatives, friend, work associate, neighbour, general practitioner, counsellor etc.) with each of the nominated persons.
Name
Date
First name or initials
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
Relationship
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ISEL
This scale is made up of a list of statements each of which may or may not be true about you. For each statement we would like you to circle TRUE if the statement is probably true about you or FALSE if the statement is probably not true about you.
You may find that many of the statements are neither clearly true or clearly false. In these cases, try to decide quickly whether TRUE or FALSE is most descriptive of you. Although some questions will be difficult to answer, it is important that you pick one alternative or the other. Remember to circle only one of the alternatives for each statement.
1. There is at least one person I know whose advice True / False
I really trust.
2. Most of my friends are more interesting than I am. True / False
3. I feel that I'm on the fringe in my circle of friends. True / False
4. I am more satisfied with my life than most people are with theirs.
True / False
5. I am able to do things as well as most other people. True / False
6. When I feel lonely, there are several people I could call and talk to.
True / False
7. There are very few people I trust to help solve my problems. True / False
8. I have someone who takes pride in my accomplishments. True / False
9. There is someone I can turn to for advice about handling hassles over household responsibilities.
True / False
10. Most people I know think highly of me. True / False
11. If I got stranded ten kilometers out of town, there is someone I could call to come and get me.
True / False
12. I think that my friends feel that I'm not very good at helping them solve problems.
True / False
13. If I needed some help in moving to a new home, I would have a hard time finding someone to help me.
•True / False
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14. If I decide on a Friday afternoon that I would like to go to a movie that evening, I could find someone to go with me.
True / False
15. I feel that there is no one with whom I can share my most private worries and fears.
True / False
16. In general, people don't have much confidence in me. True / False
17. If a family crisis arose few of my friends would be able to give me good advice about handling it.
True / False
18. When I need suggestions for how to deal with a personal problem I know there is someone I can turn to.
True / False
19. There is no one I could call on if I needed to borrow a car for a few hours.
True / False
20. There is really no one I can trust to give me good financial advice.
True / False
21. I regularly meet or talk with members of my family or friends.
True / False
22. If I need a quick emergency loan of $100, there is someone I could get it from.
True / False
23. There is someone who I feel comfortable going to for advice about sexual problems.
True / False
24. In general people do not have much confidence in me. True / False
25. If I were sick, there would be almost no one I could find to help me with my daily chores.
True / False
26. If I needed a ride to the airport very early in the morning, I would have a hard time finding anyone to take me.
True / False
27. No one I know would throw a birthday party for me. True / False
28. If for some reason I were put in jail, there is someone True / False I could call to would bail me out.
29. Most of my friends are more successful at making changes in their lives than I am.
True / False
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30. Most people I know don't enjoy the same things that I do.
True / False
31. If I were sick and needed someone to drive me to the doctor, I would have trouble finding someone.
True / False
32. There are several different people with whom I enjoy spending time.
True / False
33. If I had to mail an important letter at the post office by True / False 5:00 pm and couldn't make it, there is someone who could do it for me.
34. I don't often get invited to do things with others. True / False
35. There is someone I could turn to for advice about changing my job or finding a new one.
True / False
36. If I wanted to have lunch with someone, I could easily find someone.
True / False
37. I have a hard time keeping pace with my friends. True / False
38. If I had to go out of town for a few weeks, someone I know would look after my home (the plants, pets, yard, etc.).
True / False
39. There is really no one who can give me objective feedback about how I'm handling my problems.
True / False
40. I am closer to my friends than most other people. True / False
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Read each statement carefully. Circle the number that best describes how you feel. There are no right or wrong answers.
Not at all like me
A little like me
Somewhat like me
Very much like me
1.Once I know what I need to do, 1 2 3 4 I can do it.
2.In a new situation I expect I can handle things.
1 2 3 4
3.I am a confident person. 1 2 3 4
4.I am not very effective in solving problems. 1 2 3 4
5.When I'm stressed, I can count on myself to cope successfully. 1 2 3 4
6.I am not a self-assured person. 1 2 3 4
7.I have control over my reactions to stress.
1 2 3 4
8.I can usually get what I want. 1 2 3 4
9.I rely on my inner strength to deal with problems.
1 2 3 4
10.The good things that happen to 1 2 3 4
• me are largely my own doing.
11.I'm proud of myself. 1 2 3 4
12.I do not have a high opinion of my abilities.
1 2 3 4
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Not at all like me
A little like me
Somewhat like me
Very much like me
13. I wish I had more confidence in 1 2 3 4 my ability to succeed in life.
14. People know they can expect a 1 2 3 4 lot from me.
15. I believe I use my skills to their 1 2 3 4 best advantage.
16. I am responsible for the ways I 1 2 4 have grown as a person.
17. I can influence the people in my 1 2 3 4 life.
18. I make my interactions with 1 2 3 4 people end up the way I expect them to.
19. I am quick to learn new things 1 2 3 4 about ways to deal with problems.
20. I am not afraid to make mistakes. 1 2 3 4
21. I know what people expect from 1 2 3 4 me.
22. I question my abilities in difficult 1 2 3 4 situations.
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1 = I usually don't do this at all 2 = I usually do this a little bit 3 = I usually do this a medium amount 4 = I usually do this a lot
1. I try to grow as a person as a result of the expereince 1 2 3 4
2. I turn to work or other substitue activities to take my mind off things. 1 2 3 4
3. I get upset and let my emotions out. 1 2 3 4
4. I try to get advice from someone ablout what to do. 1 2 3 4
5. I concentrate my efforts on doing something about it. 1 2 3 4
6. I say to myself "this isn't real." 1 2 3 4
7. I put my trust in God. 1 2 3 4
8. I laugh about the situation 1 2 3 4
9. I admit to myself that I can't deal with it, and quit qucikly. 1 2 3
10. I restrain myself from doing anything too quickly. 1 2 3 4
11. I discuss my feelings with someone. 1 2 3 4
12. I use alcohol or drugs to make myself feel better. 1 2 3 4
13. I get used to the idea that it happened. 1 2 3 4
14. I talk to someone to find out more about the situation. 1 2 3 4
15. I keep myself from getting distracted by other thoughts or activities. 1 2 3 4
16. I daydream about things other than this. 1 2 3 4
17. I get upset, and am really aware of it. 1 2 3 4
18. I seek God's help. 1 2 3 4
19. I make a plan of action. 1 2 3 4
20. I make jokes about it. 1 2 3 4
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21. I accept that this has happened and that it can't be changed. 1 2 3 4
22. I hold off doing anything about it until the situation permits. 1 2 3 4
23. I try to get emotional support from frinds or relatives. 1 2 3 4
24. I just give up trying to reach my goal. 1 2 3 4
25. I take additional action to try to get rid of the problem. 1 2 3 4
26. I try to lose myself for a while by drinking alcohol or taking drugs. 1 2 3 4
27. I refuse to believe it has happened. 1 2 3 4
28. I let my feelings out. 1 2
29. I try to see it in a different light, to make it seem more positive. 1 2 3 4
30. I talk to someone who could do something concrete about the problem. 1 2 3 4
31. I sleep more than usual. 1 3 4
32. I try to come up with a strategy aboutwaht to do. 1 2 3 4
33. I focus on dealing with this problem, and if necessary let other things slide a little. 1 2 3 4
34. I get sympathy and understanding from someone. 1 2 3 4
35. I drink alcohol or take drugs, in order to think about it less. 1 2 3 4
36. I kid around about it. 1 2 3 4
37. I give up the attempt to get what I want. 1 2 3 4
38. I look for something good in waht is happening. 1 2 3 4
39. I think about how I might best handle the problem. 1 2 3 4
40. I pretend that it hasn't really happened. 1 2 3 4
41. I make sure not to make matters worse by acting too soon. 1 2 3 4
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42. I try hard to prevent other things from interfering with my efforts at dealing with this. 1 2 3 4
43. I go to movies or watch TV, to think about it less. 1 2 3 4
44. I accept the reality of the fact that it happened. 1 2 3 4
45. I ask people who have had similar experiences what they did. 1 2 3 4
46. I feel a lot of emotional dsitress and I find myself expressing those feelings alot. 1 2 3 4
47. I take direct action to get around the problem. 1 2 3 4
48. I try to find comfort in my religion. 1 2 3 4
49. I force myself to wait for the right time to do something. 1 2 3 4
50. I make fuin of the situation. 1 2 3 4
51. I reduce the amount of effort I'm putting into solving the problem. 1 2 3 4
52. I talk to someone about how I feel. 1 2 3 4
53. I use alcohol or drugs to help me get hrough it. 1 2 3 4
54. I learn to live with it. 1 2 3 4
55. I put aside other activities in order to concentrate on this. 1 2 3 4
56. I think hard about what steps to take. 1 2 3 4
57. I act as though it hasn't even happened. 1 2 3 4
58. I do what has to be done, one step at a time. 1 2 3 4
59. I learn something from the experience. 1 2 3 4
60. I pray more than usual. 1 2 3 4
